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The mechanisms regulating immune cells recruitment into the heart during healing after an acute myocardial infarction (AMI) have major clinical implications. We investigated whether cholinergic stimulation with pyridostigmine, a cholinesterase inhibitor, modulates heart and spleen immune responses and cardiac remodeling after AMI in spontaneous hypertensive rats (SHRs). Male adult SHRs underwent sham surgery or ligation of the left coronary artery and were randomly allocated to remain untreated or to pyridostigmine treatment (40 mg/kg once a day by gavage). Blood pressure and heart rate variability were determined, and echocardiography was performed at day six after MI. The heart and spleen were processed for immunohistochemistry cellular analyses (CD3+ and CD4+ lymphocytes, and CD68+ and CD206+ macrophages), and TNF levels were determined at day seven after MI. Pyridostigmine treatment increased the parasympathetic tone and T CD4+ lymphocytes in the myocardium, but lowered M1/M2 macrophage ratio towards an anti-inflammatory profile that was associated with decreased TNF levels in the heart and spleen. Treatment with this cholinergic agent improved heart remodeling manifested by lower ventricular diameters and better functional parameters. In summary, cholinergic stimulation by pyridostigmine enhances the parasympathetic tone and induces anti-inflammatory responses in the heart and spleen fostering cardiac recovery after AMI in SHRs.

Mechanisms involved in the acute responses to renal denervation (RDN) have yet to be fully understood. We assessed urinary volume, autonomic control and aorta vascular reactivity after acute RDN. Male normotensive Wistar rats and spontaneously hypertensive rats (SHR) were divided into normotensive + RDN (ND) or sham surgery (NS), and hypertensive + RDN (HD) or sham surgery (HS). Metabolic parameters and hemodynamic measurements were recorded 72h and 4 days after intervention, respectively. Aortic rings were studied 7 days post RDN in an isometric myograph. Concentration–response curves to phenylephrine, sodium nitroprusside and acetylcholine (10–10–10−5 M) were performed. Two-way ANOVA was used for group comparisons and differences reported when p vs. HS (HS = 14.94 ± 2.5 mL; HD = 31.69 ± 2.2 mL) and remained unchanged in normotensive rats. Systolic BP was lower in HD rats (HS = 201 ± 12 vs. HD = 172 ± 3 mmHg) without changes in normotensive group. HD group showed increased HF and LF modulation (HS = 5.8 ± 0.7 ms2vs. HD = 13.4 ± 1.4 ms2; HS = 3.5 ± 0.7 ms2vs. HD = 10.5 ± 1.7 ms2, respectively). RDN normalized vascular reactivity in HD rats and increased phenylephrine response in ND rats. Acute fall in BP induced by RDN is associated with increased urinary volume, which in turn may also have contributed to functional changes of the aorta.

Aim. To evaluate cardiovascular, autonomic, and oxidative stress markers in eutrophic and overweight offspring of hypertensive parents comparing them to eutrophic and overweight offspring of normotensive parents. Methods. We conducted a cross-sectional study. We selected 71 male and sedentary subjects, divided into 4 groups: eutrophic group with a negative family history of hypertension (EH-, n=18) or positive family history of hypertension (EH+, n=17), overweight group with a negative family history of hypertension (OH-, n=19) or a positive family history of hypertension (OH+, n=17), and aged between 18 and 35 years. Results. Blood glucose was higher in the OH+ group when compared to other groups. Diastolic blood pressure was increased in OH- and OH+ groups when compared to eutrophic groups. Regarding the HRV, the LF abs was higher in OH- and OH+ groups when compared to the EH- group. LF/HF values were higher in EH+ and OH+ groups when compared to the EH- and OH- groups. As to oxidative stress and the metabolism of nitric oxide, we observed an increase in hydrogen peroxide and nitrite levels in the OH+ group, and in the NADPH oxidase in OH- and OH+ groups when compared to the other groups. Conclusion. Our findings demonstrate that the overweight group with a family history of hypertension presented all the dysfunctions observed in isolation from these risk factors. We observed an exacerbation of cardiac sympathetic modulation and early prooxidants increase, which may be associated with target organ damage and cardiovascular risk in this population.

Patients undergoing coronary angiography after myocardial infarction (MI) often develop cardiac and renal dysfunction. We hypothesized that the apolipoprotein A-I mimetic peptide 4F (4F) would prevent those complications. Male Wistar rats were fed a high-cholesterol diet for 8 days. The rats were then anesthetized with isoflurane and randomly divided into five groups: a control group (sham-operated rats), and four groups of rats induced to MI by left coronary artery ligation, the rats in three of those groups being injected 6 h later, with the nonionic contrast agent iopamidol, 4F, and iopamidol plus 4F, respectively. At postprocedure hour 24, we performed the following experiments/tests ( n = 8 rats/group): metabolic cage studies; creatinine clearance studies; analysis of creatinine, urea, sodium, potassium, triglycerides, total cholesterol, very low-, low- and high-density lipoproteins (VLDL, LDL, and HDL); immunohistochemistry; histomorphometry; Western blot analysis; and transmission electron microscopy. In another set of experiments ( n = 8 rats/group), also performed at postprocedure hour 24, we measured mean arterial pressure, heart rate, heart rate variability, echocardiographic parameters, left ventricular systolic pressure, and left ventricular end-diastolic pressure. 4F protected against MI-induced increases in total cholesterol, triglycerides, and LDL; increased HDL levels; reversed autonomic and cardiac dysfunction; decreased the myocardial ischemic area; minimized renal and cardiac apoptosis; protected mitochondria; and strengthened endothelia possibly by minimizing Toll-like receptor 4 upregulation (thus restoring endothelial nitric oxide synthase protein expression) and by upregulating vascular endothelial growth factor protein expression. 4F-treated animals showed signs of cardiac neovascularization. The nitric oxide-dependent cardioprotection and renoprotection provided by 4F could have implications for post-MI treatment.

Hypertensive status induces modifications in the respiratory profile. Previous studies have indicated that hypertensive rats show increased respiratory-sympathetic coupling compared to normotensive rats. However, these effects and especially the mechanisms underlying such effects are not well known. Thus, we evaluated the influence of high blood pressure and autonomic dysfunction on a ventilatory pattern associated with lung injury and on the ubiquitin-proteasome system of the diaphragm muscle. Autonomic cardiovascular modulation (systolic BP variance and low-frequency band and pulse interval variance) and arterial blood gases patterns (pH, pO2, HCO3, SpO2), can be changed by hypertension, as well exacerbated chemoreflex pressor response. We observed that the diaphragm muscle of SHR showed increase in type I cross-sectional fiber (16%) and reduction in type II cross-sectional fiber area (41%), increased activity of the ubiquitin-proteasome system and lipid peroxidation, with no differences between groups in the analysis of ubiquitinated proteins and misfolded proteins. Our results showed that hypertension induced functional compensatory/adverse alterations associated with diaphragm fiber type changes and protein degradation as well as changed autonomic control of circulation. In conclusion, we believe there is an adaptation in ventilatory pattern in regarding to prevent the development of fatigue and muscle weakness and improve ventilatory endurance. Impact statement It was well known that hypertension can be driven by increased sympathetic activity and has been documented as a central link between autonomic dysfunction and alterations in the respiratory pattern. Our study demonstrated the impact of hypertension in ventilatory mechanics and their relationship with diaphragm muscle protein degradation. These findings may assist us in future alternative treatments to prevent diaphragm fatigue and weakness in hypertensive patients.

Histidine-containing dipeptides (HCDs) are abundantly expressed in striated muscles. Although important properties have been ascribed to HCDs, including H+ buffering, regulation of Ca2+ transients and protection against oxidative stress, it remains unknown whether they play relevant functions in vivo. To investigate the in vivo roles of HCDs, we developed the first carnosine synthase knockout (CARNS1-/-) rat strain to investigate the impact of an absence of HCDs on skeletal and cardiac muscle function. Male wild-type (WT) and knockout rats (4 months-old) were used. Skeletal muscle function was assessed by an exercise tolerance test, contractile function in situ and muscle buffering capacity in vitro. Cardiac function was assessed in vivo by echocardiography and cardiac electrical activity by electrocardiography. Cardiomyocyte contractile function was assessed in isolated cardiomyocytes by measuring sarcomere contractility, along with the determination of Ca2+ transient. Markers of oxidative stress, mitochondrial function and expression of proteins were also evaluated in cardiac muscle. Animals were supplemented with carnosine (1.8% in drinking water for 12 weeks) in an attempt to rescue tissue HCDs levels and function. CARNS1-/- resulted in the complete absence of carnosine and anserine, but it did not affect exercise capacity, skeletal muscle force production, fatigability or buffering capacity in vitro, indicating that these are not essential for pH regulation and function in skeletal muscle. In cardiac muscle, however, CARNS1-/- resulted in a significant impairment of contractile function, which was confirmed both in vivo and ex vivo in isolated sarcomeres. Impaired systolic and diastolic dysfunction were accompanied by reduced intracellular Ca2+ peaks and slowed Ca2+ removal, but not by increased markers of oxidative stress or impaired mitochondrial respiration. No relevant increases in muscle carnosine content were observed after carnosine supplementation. Results show that a primary function of HCDs in cardiac muscle is the regulation of Ca2+ handling and excitation-contraction coupling.

Background To evaluate the effect of nicotinamide prior to streptozotocin-induced (STZ) diabetes in baroreflex sensitivity and cardiovascular autonomic modulation, and its association with hemodynamics and metabolic parameters. Methods Methods: Male Wistar rats were divided into control (Cont) and STZ-induced diabetes (Diab). Half of the rats from each group received a single dose of nicotinamide (100 mg/Kg) before STZ injection (Cont+NicA and Diab+NicA). All groups were followed-up for 5 weeks. Results Body weight loss of more than 40% was observed in Diab throughout the period (Diab: 271.00 ± 12.74 g; Diab+NicA: 344.62 ± 17.82). Increased glycemia was seen in Diab rats (541.28 ± 18.68 mg/dl) while Diab+NicA group had a slight decrease (440.87 ± 20.96 mg/dl). However, insulin resistance was observed only in Diab. In relation to Cont, heart rate, mean blood pressure and diastolic function were reduced when compared to Diab, together with parasympathetic modulation and baroreflex sensitivity. All of these parameters were improved in Diab+NicA when compared to Diab. Improved baroreflex sensitivity and parasympathetic modulation were correlated with glycemia, insulin resistance, and body weight mass. Additionally, Diab+NicA group increased survival rate. Conclusions Results suggest that the association of nicotinamide in STZ-induced diabetic rats prevents most of the expected derangements mainly by preserving parasympathetic and baroreflex parameters.

Familial history of hypertension is associated with autonomic dysfunction and increase in blood pressure (BP). However, an active lifestyle has been found to improve a number of health outcomes and reduce all-cause mortality. The aim of the present study was to investigate the effects of an active lifestyle on hemodynamics, heart rate variability (HRV) and oxidative stress markers in offspring of hypertensive parents. One hundred twenty-seven subjects were assigned into four groups: sedentary offspring of normotensives (S-ON) or hypertensives (S-OH); and physically active offspring of normotensives (A-ON) or hypertensives (A-OH). Diastolic BP and heart rate were reduced in the physically active groups when compared to S-OH group. A-ON and A-OH groups presented increased values of RR total variance when compared to the sedentary ones (A-ON: 4,912 ± 538 vs. S-ON: 2,354 ± 159; A-OH: 3,112 ± 236 vs. S-OH: 2,232 ± 241 ms2). Cardiac sympato-vagal balance (LF/HF), systemic hydrogen peroxide and superoxide anion were markedly increased in S-OH group when compared to all other studied groups. Additionally, important correlations were observed between LF/HF with diastolic BP (r = 0.30) and hydrogen peroxide (r = 0.41). Thus, our findings seem to confirm an early autonomic dysfunction in offspring of hypertensive parents, which was associated with a systemic increase in reactive oxygen species and blood pressure. However, our most important finding lies in the attenuation of such disorders in offspring of physically active hypertensives, thus emphasizing the importance of a physically active lifestyle in the prevention of early disorders that may be associated with onset of hypertension.

OBJECTIVES: To evaluate the effects of sympathectomy on the myocardium in an experimental model. METHODS: The study evaluated three groups of male Wistar rats: control (CT; n=15), left unilateral sympathectomy (UNI; n=15), and bilateral sympathectomy (BIL; n=31). Sympathectomy was performed by injection of absolute alcohol into the space of the spinous process of the C7 vertebra. After 6 weeks, we assessed the chronotropic properties at rest and stress, cardiovascular autonomic modulation, myocardial and peripheral catecholamines, and beta-adrenergic receptors in the myocardium. The treadmill test consisted of an escalated protocol with a velocity increment until the maximal velocity tolerated by the animal was reached. RESULTS: The bilateral group had higher levels of peripheral catecholamines, and consequently, a higher heart rate (HR) and blood pressure levels. This suggests that the activation of a compensatory pathway in this group may have deleterious effects. The BIL group had basal tachycardia immediately before the exercise test and increased tachycardia at peak exercise (p

This study evaluated the impact of combined exercise training on the development of cardiovascular and neuroimmune complications induced by fructose consumption (10% in the drinking water) in hypertensive rats (SHR). After weaning, SHR were divided into 3 groups: SHR (H), SHR+fructose (HF) and SHR+fructose+combined exercise training (treadmill+ladder, 40–60% of maximum capacity) (HFTC). Metabolic, hemodynamic, autonomic, inflammatory and oxidative stress parameters were evaluated in the subgroups (n = 6 group/time) at 7, 15, 30 and 60 days of protocol. Fructose consumption (H vs. HF groups) decreased spontaneous baroreflex sensitivity and total variance of pulse interval at day 7 (7 to 60); increased IL-6 and TNFα in the heart (at day 15, 30 and 60) and NADPH oxidase activity and cardiac lipoperoxidation (LPO) (day 60); increased white adipose tissue weight, reduced insulin sensitivity and increased triglycerides (day 60); induced an additional increase in mean arterial pressure (MAP) (days 30 and 60). Combined exercise training prevented such dysfunctions and sustained increased cardiac IL-10 (day 7) and glutathione redox balance (GSH/GSSG) for the entire protocol. In conclusion, combined exercise training performed simultaneously with exacerbated fructose consumption prevented early cardiovascular autonomic dysfunction, probably trigging positive changes in inflammation and oxidative stress, resulting in a better cardiometabolic profile in rats genetically predisposed to hypertension.

The (pro)renin receptor [(P)RR] has been implicated as a renin/prorenin receptor, and plays a role in local renin angiotensin system activation. Our goal was to investigate whether a transgenic mouse that expresses rat tonin [TGM'(rTon)] can regulate (P)RR mRNA levels. Control (C) and TGM'(rTon) animals were subdivided into the C sham, C MI, TGM'(rTon) sham, and TGM'(rTon) MI groups. The levels of tonin, (P)RR, and renin were determined using RT-PCR mRNA. Tonin activity as determined by RIE was significantly increased in the TGM'(rTon) sham group as compared to the C sham group in the atrium (AT) and right ventricle (RV), respectively. In most mice, tonin mRNA levels were significantly reduced compared to those in the TGM'(rTon) sham group in the atria. In this structure, the (P)RR mRNA levels were statistically significantly reduced in the TGM'(rTon) sham and TGM'(rTon) MI groups compared to the control groups. However, the (P)RR mRNA values were significantly increased when we compared the TGM'(rTon) MI vs TGM'(rTon) sham groups. In the RV, the renin mRNA levels in the TGM'(rTon) sham group were significantly reduced compared to the C sham group. Tonin overexpression may act in the regulation of (P)RR mRNA levels during MI.

We tested whether aerobic exercise training (AET) would modulate the skeletal muscle protein quality control (PQC) in a model of chronic kidney disease (CKD) in rats. Adult Wistar rats were evaluated in four groups: control (CS) or trained (CE), and 5/6 nephrectomy sedentary (5/6NxS) or trained (5/6NxE). Exercised rats were submitted to treadmill exercise (60 min., five times/wk for 2 months). We evaluated motor performance (tolerance to exercise on the treadmill and rotarod), cross‐sectional area (CSA), gene and protein levels related to the unfolded protein response (UPR), protein synthesis/survive and apoptosis signalling, accumulated misfolded proteins, chymotrypsin‐like proteasome activity (UPS activity), redox balance and heat‐shock protein (HSP) levels in the tibialis anterior. 5/6NxS presented a trend towards to atrophy, with a reduction in motor performance, down‐regulation of protein synthesis and up‐regulation of apoptosis signalling; increases in UPS activity, misfolded proteins, GRP78, derlin, HSP27 and HSP70 protein levels, ATF4 and GRP78 genes; and increase in oxidative damage compared to CS group. In 5/6NxE, we observed a restoration in exercise tolerance, accumulated misfolded proteins, UPS activity, protein synthesis/apoptosis signalling, derlin, HSPs protein levels as well as increase in ATF4, GRP78 genes and ATF6α protein levels accompanied by a decrease in oxidative damage and increased catalase and glutathione peroxidase activities. The results suggest a disruption of PQC in white muscle fibres of CKD rats previous to the atrophy. AET can rescue this disruption for the UPR, prevent accumulated misfolded proteins and reduce oxidative damage, HSPs protein levels and exercise tolerance.

Increase in oxidative/nitrosative stress is one of the mechanisms associated with the development of cardiotoxicity due to doxorubicin (Dox), a potent chemotherapy drug. Previously, we reported mitigation of Dox-induced oxidative/nitrosative stress and apoptosis by vitamin C (Vit C) in isolated cardiomyocytes. In the present in vivo study in rats, we investigated the effect of prophylactic treatment with Vit C on Dox-induced apoptosis, inflammation, oxidative/nitrosative stress, cardiac dysfunction, and Vit C transporter proteins. Dox (cumulative dose: 15 mg/kg) in rats reduced systolic and diastolic cardiac function and caused structural damage. These changes were associated with a myocardial increase in reactive oxygen species, reduction in antioxidant enzyme activities, increased expression of apoptotic proteins, and inflammation. Dox also caused an increase in the expression of proapoptotic proteins Bax, Bnip-3, Bak, and caspase-3. An increase in oxidative/nitrosative stress attributable to Dox was indicated by an increase in superoxide, protein carbonyl formation, lipid peroxidation, nitric oxide (NO), NO synthase (NOS) activity, protein nitrosylation, and inducible NOS protein expression. Dox increased the levels of cardiac proinflammatory cytokines TNF-α, IL-1β, and IL-6, whereas the expression of Vit C transporter proteins (sodium-ascorbate cotransporter 2 and glucose transporter 4) was reduced. Prophylactic and concurrent treatment with Vit C prevented all these changes and improved survival in the Vit C + Dox group. Vit C also improved Dox-mediated systolic and diastolic dysfunctions and structural damage. These results suggest a cardioprotective role of Vit C in Dox-induced cardiomyopathy by reducing oxidative/nitrosative stress, inflammation, and apoptosis, as well as improving Vit C transporter proteins. NEW & NOTEWORTHY This in vivo study provides novel data that vitamin C improves cardiac structure and function in doxorubicin-induced cardiomyopathy by reducing oxidative/nitrosative stress, apoptosis, and inflammation along with upregulation of cardiac vitamin C transporter proteins. The latter may have a crucial role in improving antioxidant status in this cardiomyopathy.

Angiotensin-(1-7) counterbalances angiotensin II cardiovascular effects. However, it has yet to be determined how cardiovascular autonomic modulation may be affected by chronic and acute elevation of Ang-(1-7). Hemodynamics and cardiovascular autonomic profile were evaluated in male Sprague-Dawley (SD) rats and transgenic rats (TGR) overexpressing Ang-(1-7) [TGR(A1-7)3292]. Blood pressure (BP) was directly measured while cardiovascular autonomic modulation was evaluated by spectral analysis. TGR received A-779 or vehicle and SD rats received Ang-(1-7) or vehicle and were monitored for 5 h after i.v. administration. In another set of experiments with TGR, A-779 was infused for 7 days using osmotic mini pumps. Although at baseline no differences were observed, acute administration of A-779 in TGR produced a marked long-lasting increase in BP accompanied by increased BP variability (BPV) and sympathetic modulation to the vessels. Likewise, chronic administration of A-779 with osmotic mini pumps in TGR increased heart rate, sympathovagal balance, BPV, and sympathetic modulation to the vessels. Administration of Ang-(1-7) to SD rats increased heart rate variability values in 88% accompanied by 8% of vagal modulation increase and 18% of mean BP reduction. These results show that both acute and chronic alteration in the Ang-(1-7)-Mas receptor axis may lead to important changes in the autonomic control of circulation, impacting either sympathetic and (or) parasympathetic systems.

In acute myocardial infarction (AMI), reactive oxygen species may cause irreversible damage to the heart tissue. Physical training is capable of enhancing antioxidant capacity, acting as a cardioprotective factor. We assessed the preventive effects of physical training on the antioxidant and functional responses of the heart of Wistar Kyoto rats after AMI. Wistar Kyoto rats (n = 12) were allocated to sedentary (SED) or trained (EXE—aerobic training on a treadmill) groups. Echocardiographic exams were performed 48 hr before and 48 hr after the induction of AMI. Superoxide dismutase (SOD) and catalase (CAT) activities, and total glutathione (GSH) were measured in vitro in the heart tissue. After AMI, the EXE group showed higher left ventricular shortening fraction (29%; p = .004), higher cardiac output (37%; p = .032) and reduced myocardial infarction size (16%; p = .007) than SED. The EXE group showed a higher nonenzymatic antioxidant capacity (GSH, 23%; p = .004), but the SOD and CAT activities were higher in SED (23% SOD; p = .021 and 20% CAT; p = .016). In addition, the SOD activity was positively correlated with myocardial infarction size and inversely correlated with cardiac output. Physical training partially preserved cardiac function and increased intracellular antioxidant response in cardiac tissue of animals after AMI.

Background The effects of exercise training (ET) associated with pyridostigmine bromide (PYR) treatment on cardiac and autonomic function, as well as on inflammatory profile after myocardial infarction (MI), are unclear. Methods Male Wistar rats were randomly assigned to: control (C); sedentary+infarcted (I); sedentary+infarcted treated with PYR (IP); infarcted submitted to aerobic exercise training (IT); and infarcted submitted to treatment with PYR and aerobic exercise training (ITP). After 12weeks of ET (50–70% maximal running speed; 1h a day, 5days a week) and/or PYR treatment (0.14mg/mL on drink water), hemodynamic, autonomic and cytokines expression were performed. Results We observed that both aerobic ET, associated or not with PYR treatment in MI animals, were able to: reduced MI area, improved systolic and diastolic function, baroreflex sensitivity, cardiovascular autonomic modulation, and tonic activity of the sympathetic and parasympathetic nervous system. Also, they led to a reduction of inflammatory profile measured at plasma, left ventricle and soleus skeletal muscle. However, additional effects were observed when ET and PYR were associated, such as an increase in vagal tonus and modulation, reduction of MI area, interferon-γ and tumor necrosis factor-α (TNF-α), as well as an increase of interleukin-10/TNF-α ratio on left ventricle. Conclusion These data suggest that associating ET and PYR promotes some additional benefits on cardiovascular autonomic modulation and inflammatory profile in infarcted rats.

Sepsis induces organ dysfunction due to overexpression of the inflammatory host response, resulting in cardiopulmonary and autonomic dysfunction, thus increasing the associated morbidity and mortality. Wharton’s jelly-derived mesenchymal stem cells (WJ-MSCs) express genes and secrete factors with anti-inflammatory properties, neurological and immunological protection, as well as improve survival in experimental sepsis. The cholinergic anti-inflammatory pathway (CAP) is mediated by α7-nicotinic acetylcholine receptors (α7nAChRs), which play an important role in the control of systemic inflammation. We hypothesized that WJ-MSCs attenuate sepsis-induced organ injury in the presence of an activated CAP pathway. To confirm our hypothesis, we evaluated the effects of WJ-MSCs as a treatment for cardiopulmonary injury and on neuroimmunomodulation. Male Wistar rats were randomly divided into four groups: control (sham-operated); cecal ligation and puncture (CLP) alone; CLP+WJ-MSCs (1 × 106 cells, at 6 h post-CLP); and CLP+methyllycaconitine (MLA)+WJ-MSCs (5 mg/kg body wt, at 5.5 h post-CLP, and 1 × 106 cells, at 6 h post-CLP, respectively). All experiments, including the assessment of echocardiographic parameters and heart rate variability, were performed 24 h after CLP. WJ-MSC treatment attenuated diastolic dysfunction and restored baroreflex sensitivity. WJ-MSCs also increased cardiac sympathetic and cardiovagal activity. WJ-MSCs reduced leukocyte infiltration and proinflammatory cytokines, effects that were abolished by administration of a selective α7nAChR antagonist (MLA). In addition, WJ-MSC treatment also diminished apoptosis in the lungs and spleen. In cardiac and splenic tissue, WJ-MSCs downregulated α7nAChR expression, as well as reduced the phospho-STAT3-to-total STAT3 ratio in the spleen. WJ-MSCs appear to protect against sepsis-induced organ injury by reducing systemic inflammation, at least in part, via a mechanism that is dependent on an activated CAP.

SUMMARY BACKGROUND: The use of the 3D printer in complex cardiac surgery planning. OBJECTIVES: To analyze the use and benefits of 3D printing in heart valve surgery through a systematic review of the literature. METHODS: This systematic review was reported following the Preferred Reporting Items for Systematic Review and registered in the Prospero (International Prospective Register of Systematic Reviews) database under the number CRD42017059034. We used the following databases: PubMed, EMBASE, Scopus, Web of Science and Lilacs. We included articles about the keywords “Heart Valves”, “Heart Valve Prosthesis Implantation”, “Heart Valve Prosthesis”, “Printing, Three-Dimensional”, and related entry terms. Two reviewers independently conducted data extraction and a third reviewer solved disagreements. All tables used for data extraction are available at a separate website. We used the Cochrane Collaboration tool to assess the risk of bias of the studies included. RESULTS: We identified 301 articles and 13 case reports and case series that met the inclusion criteria. Our studies included 34 patients aged from 3 months to 94 years. CONCLUSIONS: Up to the present time, there are no studies including a considerable number of patients. A 3D-printed model produced based on the patient enables the surgeon to plan the surgical procedure and choose the best material, size, format, and thickness to be used. This planning leads to reduced surgery time, exposure, and consequently, lower risk of infection.

PURPOSE: To investigate the myocardial ischemia-reperfusion with sevoflurane anesthetic preconditioning (APC) would present beneficial effects on autonomic and cardiac function indexes after the acute phase of a myocardial ischemia-reperfusion. METHODS: Twenty Wistar rats were allocated in three groups: control (CON, n=10), myocardial infarction with sevoflurane (SEV, n=5) and infarcted without sevoflurane (INF, n=5). Myocardial ischemia (60 min) and reperfusion were performed by temporary coronary occlusion. Twenty-one days later, the systolic and diastolic function were evaluated by echocardiography; spectral analysis of the systolic arterial pressure (SAPV) and heart rate variability (HRV) were assessed. After the recording period, the infarct size (IS) was evaluated. RESULTS: The INF group presented greater cardiac dysfunction and increased sympathetic modulation of the SAPV, as well as decreased alpha index and worse vagal modulation of the HRV. The SEV group exhibited attenuation of the systolic and diastolic dysfunction and preserved vagal modulation (square root of the mean squared differences of successive R-R intervals and high frequency) of HRV, as well as a smaller IS. CONCLUSION: Sevoflurane preconditioning better preserved the cardiac function and autonomic modulation of the heart in post-acute myocardial infarction period.

Family history of hypertension is an important predictive factor for hypertension and is associated with hemodynamic and autonomic abnormalities. Previous studies reported that strength training might reduce arterial blood pressure (AP), as well as improve heart rate variability (HRV). However, the benefits of strength training in the offspring of hypertensive parents have not been fully evaluated. Here, we analyzed the impact of strength training on hemodynamics and autonomic parameters in offspring of hypertensive subjects. We performed a cross-sectional study with sedentary or physically active offspring of normotensives (S-ON and A-ON) or hypertensives (S-OH and A-OH). We recorded RR interval for analysis of HRV. AP was similar between groups. Sedentary offspring of hypertensives presented impairment of total variance of RR interval, as well as an increase in cardiac sympathovagal balance (S-OH: 4.2±0.7 vs S-ON: 2.8±0.4 and A-ON: 2.4±0.1). In contrast, the strength-trained group with a family history of hypertension did not show such dysfunctions. In conclusion, sedentary offspring of hypertensives, despite displaying no changes in AP, showed reduced HRV, reinforcing the hypothesis that autonomic dysfunctions have been associated with higher risk of hypertension onset. Our findings demonstrated that strength-trained offspring of hypertensives did not present impaired HRV, thus reinforcing the benefits of an active lifestyle in the prevention of early dysfunctions associated with the onset of hypertension in predisposed populations.

Inflammatory processes and cardiovascular autonomic imbalance are very relevant characteristic of the enormous dynamic process that is a myocardial infarction (MI). In this sense, some studies are investigating pharmacological therapies using acetylcholinesterase inhibitors, such as pyridostigmine bromide (PYR), aiming to increase parasympathetic tone after MI. Here we hypothesized that the use of PYR before the MI might bring an additional positive effect to the autonomic function, and consequently, in the inflammatory response and cardiac function. The present study aimed to evaluate left ventricular function, baroreflex sensitivity, autonomic modulation, and inflammatory profile in PYR-treated rats previously to MI. Methods: Male Wistar rats (250–300 g) were treated for 60 days with PYR. After treatment, they were submitted to the MI. After the MI, the autonomic and ventricular function were evaluated, as well as the systemic, left ventricle, and adipose tissue inflammatory profile. Results: PYR, performed before MI, prevented HR increase, systolic function impairment, baroreflex sensitivity drop, as well as pulse interval variance, RMSSD, blood pressure and parasympathetic modulation reduction in treated rats compared to untreated rats. Also, this positive functional changes may have been a result of the reduced inflammatory parameters in the left ventricle (IFN-γ, IL-6, and IL-1β), as well as increased IL-10 expression and IL-10/TNF-α ratio in treated animals before MI. Conclusion: Prior treatment with PYR prevents impairment of the autonomic nervous system after MI, which may be associated with the attenuated expression of inflammatory factors and heart dysfunction.

Tele-electrocardiography (tele-ECG) is a powerful ally in the screening of acute ischemic lesions.Evidence that confirms the correlation between the diagnosis of acute coronary syndrome (ACS) determined in the prehospital setting and the confirmation of the diagnosis in the hospital setting is scarce. This study compares the presumed diagnosis of ACS in the prehospital setting based on electrocardiographic changes, such as ST-segment deviation, with the diagnosis confirmed in a hospital setting.Retrospective, cross-sectional analysis of medical records of patients who sought emergency ambulance services of a distinguished public healthcare service in the city of Porto Alegre from September 2013 to August 2014. Data were collected from tele-ECG recordings and medical records available at the database of the Secretary of Health. The study was based on the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) guidelines.Among the 1,338 prehospital examinations performed, a total of 250 admissions in tertiary hospitals were registered. There was a significant agreement (p 0.01) of 71% of the electrocardiographic changes identified in the prehospital setting with the diagnosis of ACS confirmed in the hospital setting. These changes were more prevalent in men (p = 0.048) and in patients aged 60 years or older (p = 0.006).The tele-ECG allows the early diagnosis of ACS, reducing the delay to definitive treatment, be it reperfusion, chemical, or mechanical therapy.Seventy-two percent of the prehospital diagnosis of ACS based on electrocardiographic changes was later confirmed in the hospital setting.

Patients on hemodialysis (HD) are at increased risk for arrhythmias and sudden cardiac death. Autonomic nervous system (ANS) dysfunction seems to participate in the arrhythmogenic process. Genetic factors have an impact on ANS modulation, but the specific role of the insertion/deletion (I/D) polymorphism in the gene for angiotensin-converting enzyme (ACE) has not been investigated. Since the D allele increases gene expression, it is a candidate polymorphism to interact with the ANS. The aim of the present study was to compare the behavior of heart rate variability (HRV) during HD, as a surrogate for ANS response to stressors, between the ACE genotypes. In a sample of patients with chronic kidney disease I/D ACE genotypes were assessed with PCR and HRV was measured before, in the second hour, and after a HD session. HRV parameters in the time and frequency domains were analyzed by repeated-measures mixed models according to the time of measurement and ACE polymorphism. HRV parameters in the frequency domain presented significantly different variations during the HD session between patients with or without the D allele. Only patients with the II genotype presented an increase in low-frequency normalized units and in the low frequency-to-high frequency ratio throughout HD. Patients with the II genotype seemed to have a more physiological response to the volemic and electrolytic changes that occur during HD, with greater sympathetic activation than patients with ID and DD genotypes.NEW & NOTEWORTHY Adding to the effort to understand the complexity of cardiovascular system regulation, we have found that the autonomic nervous system response to the acute volume removal during hemodialysis may be different between angiotensin-converting enzyme insertion/deletion polymorphisms. To our knowledge, this is the first time that this specific interaction was analyzed during a volume removal intervention.

Background: Stress is a state of threat to the balance of the organism, which can cause biological and psychological changes. In hypertensive patients, stress can interfere with blood pressure levels, influence on food choices and neglect of the diet. Objective: This study aims to describe the relationship between stress and dietary intake of hypertensive patients. Methods: A transversal study was carried out at the Arterial Hypertension Clinic of the Cardiology Institute of Rio Grande do Sul, Brazil. The participants were aged ≥ 18 years and hypertensive. Blood pressure, food consumption and anthropometric measurements were collected. The variables related to stress were evaluated by the Lipp’s Stress Symptoms Inventory (LSSI) for adults. Significance level of 5% has been considered for all analyzed data. Results: The number of participants was 100. There was a higher prevalence of the female sex (67%), the mean age of the study population was 55.87 ± 12.55 years. Among the participants, 86% were classified in some of the stress phases, on which 57% were in the resistance phase. It was observed that there was no correlation between the presence of stress (as well as their actions), pressure levels and food consumption. The consumption of foods rich in lipids and individuals with a prevalence of psychological symptoms of stress displayed a significant association. Conclusions: Rich in fat dietary has been the first choice in patients with psychological symptoms of stress. Further studies regarding remodeled dietary intake and blood pressure levels in relation to the stress phases are suggested. These findings are important to contribute to the development of prevention and treatment strategies for cardiovascular diseases. Resumo Fundamento: O estresse é um estado de ameaça ao equilíbrio do organismo, podendo causar alterações biológicas e psicológicas. No paciente hipertenso o estresse pode interferir nos níveis pressóricos e gerar influência nas escolhas alimentares e negligência da dieta. Objetivo: Este estudo tem como objetivo descrever a relação entre o estresse e consumo alimentar de pacientes hipertensos. Métodos: Estudo transversal, desenvolvido no Ambulatório de Hipertensão Arterial do Instituto de Cardiologia do Rio Grande do Sul. Participaram da pesquisa indivíduos hipertensos com idade > 18 anos. Foram coletados dados de pressão arterial, consumo alimentar e medidas antropométricas. As variáveis relacionadas ao estresse foram avaliadas pelo inventário de sintomas de stress para adultos de Lipp (ISSL). Em todas as análises foi considerando um nível de significância 5% (p < 0,05). Resultados: O número de participantes foi de 100. Houve maior prevalência no sexo feminino (67%), a idade média da população estudada foi 55,87 ± 12,55 anos. Dos participantes, 86% se classificaram em alguma das fases do estresse, sendo que destes, 57% estavam na fase de resistência. Observou-se que não houve correlação entre a presença de estresse (bem como suas fases), níveis pressóricos e consumo alimentar. O consumo de alimentos ricos em lipídios em hipertensos com sintomas de estresse apresentou significância estatística. Conclusão: Os alimentos ricos em gordura prevaleceram entre as escolhas alimentares nos pacientes com sintomas psicológicos de estresse. Sugere-se mais estudos em relação a alteração do consumo alimentar e níveis pressóricos em relação às fases do estresse.

This study analyzes whether autonomic dysfunction precedes cardiometabolic alterations in spontaneously hypertensive rats (SHR) with fructose overload. Animals were randomly distributed into three groups: control, hypertensive and hypertensive with fructose overload. Fructose overload (100 g/L) was initiated at 30 days old, and the animals (n = 6/group/time) were evaluated after 7, 15, 30 and 60 days of fructose consumption. Fructose consumption reduced baroreflex sensitivity by day 7, and still induced a progressive reduction in baroreflex sensitivity over the time. Fructose consumption also increased TNFα and IL-6 levels in the adipose tissue and IL-1β levels in the spleen at days 15 and 30. Fructose consumption also reduced plasmatic nitrites (day 15 and 30) and superoxide dismutase activity (day 15 and 60), but increased hydrogen peroxide (day 30 and 60), lipid peroxidation and protein oxidation (day 60). Fructose consumption increased arterial pressure at day 30 (8%) and 60 (11%). Fructose consumption also induced a late insulin resistance at day 60, but did not affect glucose levels. In conclusion, the results show that baroreflex sensitivity impairment precedes inflammatory and oxidative stress disorders, probably by inducing hemodynamic and metabolic dysfunctions observed in metabolic syndrome.

SUMMARY BACKGROUND The Medical Control Program for Occupational Health establishes the required supplementary exams, according to the activity exercised by the worker and its inherent risks. The Regulatory Norm No. 35, recently deployed, stipulates that at-height workers must undergo electrocardiogram exams as an additional routine examination. OBJECTIVE To evaluate the electrocardiographic standard in at-height. METHODOLOGY A cross-sectional study, developed from May 2014 to January 2015 with male at-height workers. Anthropometric and clinical data were collected after the electrocardiogram (ECG). The workers included in the program were evaluated by an occupational medicine service of Serra Gaúcha, responsible for medical assessment and occupational tests. All workers were assessed by the researcher. RESULTS A total of 561 at-height workers participated in the study. The average age was 35.9 ± 12.2 years. A total of 176 (31%) presented electrocardiographic changes in the analysis of the resting ECG. Regarding the amendments in the resting ECG, 15.7% were attributed to changes in ventricular repolarization, 8% as blocks conductions, and 5.8% as left ventricular overload. Demographic variables were not associated with changes in the electrocardiographic tracing CONCLUSION This study demonstrated the electrocardiographic alterations and the profile of at-height workers. These findings can help determine prevention strategies and provide warnings of possible future harms to the health of these workers. RESUMO FUNDAMENTO O Programa de Controle Médico e Saúde Ocupacional estabelece a realização de exames complementares de acordo com a atividade exercida pelo trabalhador e os riscos a ela inerentes. A Norma Regulamentadora n0 35, implantada recentemente, estabelece que trabalhadores que exercem funções em altura realizem o eletrocardiograma como um exame complementar de rotina. OBJETIVO Avaliar o padrão eletrocardiográfico dos trabalhadores em altura por meio da realização do ECG de repouso. MÉTODOS Estudo transversal, desenvolvido de maio de 2014 a janeiro de 2015 com trabalhadores masculinos que exercem funções em altura. Foram coletados dados clínicos e demográficos e, após, realizado o eletrocardiograma (ECG). Os trabalhadores incluídos eram vinculados a um serviço de medicina do trabalho da Serra Gaúcha, destinado à realização de avaliação médica e exames ocupacionais. Todos foram avaliados pela pesquisadora. RESULTADOS Participaram 561 trabalhadores em altura. A média de idade foi de 35,9±12,2 anos, e 176 (31%) apresentaram alterações eletrocardiográficas na análise dos ECG de repouso. Das alterações do ECG de repouso, 15,7% foram atribuídas a alterações da repolarização ventricular; 8% como bloqueios de condução e 5,8% como sobrecarga de ventrículo esquerdo. As variáveis demográficas não estavam associadas com alterações no traçado eletrocardiográfico. CONCLUSÃO Este estudo verificou que a prevalência de sobrecarga de ventrículo esquerdo e alteração da repolarização ventricular, nos trabalhadores em altura, é maior quando comparada a estudos populacionais brasileiros. A associação de fatores de risco e alterações eletrocardiográficas em indivíduos difere de populações específicas.

The present study aimed to study the effects of exercise training (ET) performed by rats on a 10-week high-fructose diet on metabolic, hemodynamic, and autonomic changes, as well as intraocular pressure (IOP). Male Wistar rats receiving fructose overload in drinking water (100 g/L) were concomitantly trained on a treadmill for 10 weeks (FT group) or kept sedentary (F group), and a control group (C) was kept in normal laboratory conditions. The metabolic evaluation comprised the Lee index, glycemia, and insulin tolerance test (KITT). Arterial pressure (AP) was measured directly, and systolic AP variability was performed to determine peripheral autonomic modulation. ET attenuated impaired metabolic parameters, AP, IOP, and ocular perfusion pressure (OPP) induced by fructose overload (FT vs F). The increase in peripheral sympathetic modulation in F rats, demonstrated by systolic AP variance and low frequency (LF) band (F: 37±2, 6.6±0.3 vs C: 26±3, 3.6±0.5 mmHg2), was prevented by ET (FT: 29±3, 3.4±0.7 mmHg2). Positive correlations were found between the LF band and right IOP (r=0.57, P=0.01) and left IOP (r=0.64, P=0.003). Negative correlations were noted between KITT values and right IOP (r=-0.55, P=0.01) and left IOP (r=-0.62, P=0.005). ET in rats effectively prevented metabolic abnormalities and AP and IOP increases promoted by a high-fructose diet. In addition, ocular benefits triggered by exercise training were associated with peripheral autonomic improvement.

We previously reported that cholinergic stimulation with pyridostigmine (PY) induces anti-inflammatory cell recruitment soon after myocardial infarction (MI). In this study, we evaluated the anti-inflammatory effects of PY during the proliferative phase of cardiac repair by analyzing the infiltration of macrophages, Treg lymphocytes, oxidative stress and inflammatory cytokines. Wistar rats underwent control sham surgery or ligation of the left coronary artery and were randomly allocated to remain untreated (untreated infarcted group, I) or to receive PY (30 mg·kg(-1)·day(-1)) in the supplied water (infarcted treated group, I + PY). Blood pressure and heart rate variability were registered at day 5 post-MI. The animals were euthanized 7 days after thoracotomy, when the hearts were removed and processed for immunohistochemistry (CD68, CD206, FOXP3), cytokines (IL-1β, IL-6, IL-10, TNF-α) and oxidative stress (superoxide dismutase, catalase, glutathione peroxidase, lipidic and protein peroxidation). PY treatment increased parasympathetic modulation, M2 macrophages and the anti-oxidant enzyme activity but reduced protein oxidation (carbonyls) and the concentration of IL-1β, IL-6, TNF-α and IL-10. Cholinergic stimulation induces parasympathetic neuro-immune modulation and anti-inflammatory cell enrollment as well as prevents oxidative stress and cytokine production after MI. Fil: Bezerra, Otávio C.. Universidade Nove de Julho; Brasil Fil: França, Cristiane Miranda. Universidade Nove de Julho; Brasil. Oregon Health and Science University; Estados Unidos Fil: Rocha, Juraci Aparecida. Universidade de Sao Paulo; Brasil Fil: Neves, Gizele A.. Universidade Nove de Julho; Brasil Fil: Souza, Pamella Ramona M.. Universidade Nove de Julho; Brasil Fil: Teixeira Gomes, Mariana. Universidade Nove de Julho; Brasil Fil: Malfitano, Christiane. Universidade de Sao Paulo; Brasil Fil: Loleiro, Tatiane C. Alba. Universidade de Sao Paulo; Brasil Fil: Dourado, Paulo Magno. Universidade de Sao Paulo; Brasil Fil: Llesuy, Susana Francisca. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: De Angelis, Katia. Universidade Nove de Julho; Brasil Fil: Irigoyen, Maria Claudia C.. Universidade de Sao Paulo; Brasil Fil: Ulloa, Luis. New Jersey Medical School; Estados Unidos Fil: Consolim Colombo, Fernanda M.. Universidade Nove de Julho; Brasil. Universidade de Sao Paulo; Brasil

Approximately 30% of the chronic kidney disease patients using recombinant human erythropoietin (rhuEPO) have an increase in blood pressure (BP). Its mechanism and whether it depends on renal function remain unclear. There is early evidence that acetylsalicylic acid (ASA) prevents the rhuEPO-induced increase in BP. This study aims to verify whether very high doses of rhuEPO can increase BP in nonuremic rats and whether the co-administration of ASA can prevent it.Forty male Wistar rats were divided into four groups: placebo/placebo; placebo/rhuEPO 200 UI/kg thrice weekly; placebo/ASA 50 mg/kg daily; rhuEPO 200 UI/kg thrice weekly/ASA 50 mg/kg daily. Hematocrit was measured before and after and systolic BP was measured weekly by tail-cuff technique. Direct measurement of the BP was obtained at the end.The rhuEPO groups had higher final hematocrit (rhuEPO/placebo 56.7 ± 7.6, rhuEPO/ASA 56.7 ± 7.7; p0.001 versus placebo/placebo, 42.2 ± 4.7 and ASA/placebo 41.2 ± 4.2); and also increase in systolic BP (rhuEPO/placebo 135.1 ± 15.0, p = 0.01 and rhuEPO/ASA 127.2 ± 6.8, p = 0.02), whereas BP in rats from placebo/placebo (120.9 ± 5.0, p = 0.18) and placebo/ASA (124.6 ± 13.3, p = 0.12) groups remained unchanged. By direct measurement, the final BP was higher in rhuEPO/placebo (DBP 123.1 ± 12.0; SBP 157.4 ± 12.5; MBP 139.8 ± 11.9) than placebo/placebo (DBP 105.1 ± 11.5; SBP 141.0 ± 12.6; MBP 122.1 ± 12.1) and placebo/ASA groups (DBP 106.6 ± 8.1; SBP 141.5 ± 8.4, MBP 122.1 ± 7.2) (p0.05 by post hoc Bonferroni test ANOVA). The rhuEPO/ASA group (PAD 115.1 ± 11.4, PAS 147.4 ± 9.1, MBP 130.1 ± 10.3) was not different from other groups.The administration of very high doses of rhuEPO is associated with an increase in hematocrit and BP in nonuremic rats. The concomitant use of ASA mitigates the rhuEPO-associated BP increase.

Background: Although resistance exercise training is part of cardiovascular rehabilitation programs, little is known about its role on the cardiac and autonomic function after myocardial infarction. Objective: To evaluate the effects of resistance exercise training, started early after myocardial infarction, on cardiac function, hemodynamic profile, and autonomic modulation in rats. Methods: Male Wistar rats were divided into four groups: sedentary control, trained control, sedentary infarcted and trained infarcted rats. Each group with n = 9 rats. The animals underwent maximum load test and echocardiography at the beginning and at the end of the resistance exercise training (in an adapted ladder, 40% to 60% of the maximum load test, 3 months, 5 days/week). At the end, hemodynamic, baroreflex sensitivity and autonomic modulation assessments were made. Results: The maximum load test increased in groups trained control (+32%) and trained infarcted (+46%) in relation to groups sedentary control and sedentary infarcted. Although no change occurred regarding the myocardial infarction size and systolic function, the E/A ratio (-23%), myocardial performance index (-39%) and systolic blood pressure (+6%) improved with resistance exercise training in group trained infarcted. Concomitantly, the training provided additional benefits in the high frequency bands of the pulse interval (+45%), as well as in the low frequency band of systolic blood pressure (-46%) in rats from group trained infarcted in relation to group sedentary infarcted. Conclusion: Resistance exercise training alone may be an important and safe tool in the management of patients after myocardial infarction, considering that it does not lead to significant changes in the ventricular function, reduces the global cardiac stress, and significantly improves the vascular and cardiac autonomic modulation in infarcted rats. Fundamento: Embora o treinamento físico resistido esteja inserido nos programas de reabilitação cardiovascular, pouco se sabe sobre seu papel isolado na função cardíaca e autonômica após o infarto do miocárdio. Objetivo: Avaliar os efeitos do treinamento físico resistido iniciado precocemente após o infarto do miocárdio na função cardíaca, no perfil hemodinâmico e na modulação autonômica de ratos. Métodos: Ratos Wistar machos foram divididos em Grupos Controle Sedentário, Controle Treinado, Infartado Sedentário e Infartado Treinado. Cada grupo foi composto por 9 ratos. Os animais realizaram o teste de carga máxima e a ecocardiografia ao início e ao final do treinamento físico resistido (em escada adaptada, 40 a 60% do teste de carga máxima, 3 meses, 5 dias/semana). Ao final, foram realizadas avaliações hemodinâmicas, de sensibilidade barorreflexa e da modulação autonômica. Resultados: O teste de carga máxima aumentou nos Grupos Controle Treinado (+32%) e Infartado Treinado (+46%) em relação aos Grupos Controle Sedentário e Infartado Sedentário. Embora a área de infarto do miocárdio e a função sistólica não tenham sido alteradas, a relação E/A (-23%), o índice de desempenho miocárdico (-39%) e a pressão arterial sistólica (+6%) foram melhorados pelo treinamento físico resistido no Grupo Infartado Treinado. Paralelamente, o treinamento induziu os grupos a benefícios adicionais nas bandas de alta frequência do intervalo de pulso (+45%), bem como a banda de baixa frequência da pressão arterial sistólica (-46%) nos ratos do Grupo Infartado Treinado em relação aos do Infartado Sedentário. Conclusão: O treinamento físico resistido dinâmico de intensidade baixa/moderada pode ser uma importante e segura ferramenta no manejo de pacientes após infarto do miocárdio, tendo em vista que não promove mudanças expressivas da função ventricular, reduz o estresse cardíaco global e melhora significativamente a modulação autonômica cardíaca e vascular em ratos infartados.

Transcutaneous electrical nerve stimulation (TENS) is a type of therapy used primarily for analgesia, but also presents changes in the cardiovascular system responses; its effects are dependent upon application parameters. Alterations to the cardiovascular system suggest that TENS may modify venous vascular response. The objective of this study was to evaluate the effects of TENS at different frequencies (10 and 100 Hz) on venous vascular reactivity in healthy subjects. Twenty-nine healthy male volunteers were randomized into three groups: placebo (n=10), low-frequency TENS (10 Hz, n=9) and high-frequency TENS (100 Hz, n=10). TENS was applied for 30 min in the nervous plexus trajectory from the superior member (from cervical to dorsal region of the fist) at low (10 Hz/200 μs) and high frequency (100 Hz/200 μs) with its intensity adjusted below the motor threshold and intensified every 5 min, intending to avoid accommodation. Venous vascular reactivity in response to phenylephrine, acetylcholine (endothelium-dependent) and sodium nitroprusside (endothelium-independent) was assessed by the dorsal hand vein technique. The phenylephrine effective dose to achieve 70% vasoconstriction was reduced 53% (P

The autonomic nervous system (ANS) has an important role in physical performance. However, the cardiac ANS activity in high-level track and field athletes has been poorly explored. Thus, we tested the hypothesis that endurance and power athletes would present a markedly different cardiac autonomic control at rest. We analyzed the cardiac ANS by means of time and frequency domains heart rate variability (HRV) analyses and by symbolic analysis. Endurance athletes showed higher pulse interval than power athletes (1,265±126 vs. 1,031±98 ms respectively; p0.05). No differences were found in time and frequency domains between the groups. However, the LF%, HF% and LF/HF ratio presented high effect sizes (1.46, 1.46 and 1.30, respectively). The symbolic analysis revealed that endurance athletes had higher 2V parasympathetic modulation (36±6.5) than power athletes (24±9.3; p0.05). A reduced 0V sympathetic modulation was observed in endurance athletes (21±9.9) compared to power athletes (33±11; p0.05 and ES=1.30). Our results suggest greater parasympathetic modulation and less sympathetic modulation in endurance athletes compared to power athletes. Additionally, the type of HRV analysis needs to be chosen with well-defined criteria and caution because their use in assessing cardiac autonomic modulation can interfere with the interpretation of results. In practical terms, symbolic analysis appears to better discriminate between cardiac autonomic activities of athletes with different training backgrounds than frequency domain analysis.

Low angiotensin-(1-7) (Ang-(1-7)) concentration is observed in some cardiovascular diseases and exercise training seems to restore its concentration in the heart. Recently, a novel formulation of an orally active Ang-(1-7) included in hydroxy-propyl-beta-cyclodextrin (HPB-CD) was developed and chronically administered in experimental models of cardiovascular diseases. The present study examined whether chronic administration of HPB-CD/Ang-(1-7) produces beneficial cardiovascular effects in spontaneously hypertensive rats (SHR), as well as to compare the results obtained with those produced by exercise training. Male SHR (15-week old) were divided in control (tap water) or treated with HPB-CD/Ang-(1-7) (corresponding to 30μgkg(-1)day(-1) of Ang-(1-7)) by gavage, concomitantly or not to exercise training (treadmill, 10 weeks). After chronic treatment, hemodynamic, morphometric and molecular analysis in the heart were performed. Chronic HPB-CD/Ang-(1-7) decreased arterial blood pressure (BP) and heart rate in SHR. The inclusion compound significantly improved left ventricular (LV) end-diastolic pressure, restored the maximum and minimum derivatives (dP/dT) and decreased cardiac hypertrophy index in SHR. Chronic treatment improved autonomic control by attenuating sympathetic modulation on heart and vessels and the SAP variability, as well as increasing parasympathetic modulation and HR variability. Overall results were similar to those obtained with exercise training. These results show that chronic treatment with the HPB-CD/Ang-(1-7) inclusion compound produced beneficial effects in SHR resembling the ones produced by exercise training. This observation reinforces the potential cardiovascular therapeutic effect of this novel peptide formulation.

Made available in DSpace on 2014-12-03T13:11:39Z (GMT). No. of bitstreams: 0 Previous issue date: 2014-01-01Bitstream added on 2014-12-03T13:22:31Z : No. of bitstreams: 1 WOS000338068400001.pdf: 2981557 bytes, checksum: 769e6c6d76deabe0ad56ded3c9611428 (MD5) Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) The aim of this study was to evaluate the effects of exercise training (ET, 50-70% of VO2max, 5 days/week) and detraining (DT) on inflammatory and metabolic profile after myocardial infarction (MI) in rats. Male Wistar rats were divided into control (C, n = 8), sedentary infarcted (SI, n = 9), trained infarcted (TI, n = 10; 3 months of ET), and detrained infarcted (DI, n = 11; 2 months of ET + 1 month of DT). After ET and DT protocols, ventricular function and inflammation, cardiovascular autonomic modulation (spectral analysis), and adipose tissue inflammation and lipolytic pathway were evaluated. ET after MI improved cardiac and vascular autonomic modulation, and these benefits were correlated with reduced inflammatory cytokines on the heart and adipose tissue. These positive changes were sustained even after 1 month of detraining. No expressive changes were observed in oxidative stress and lipolytic pathway in experimental groups. In conclusion, our results strongly suggest that the autonomic improvement promoted by ET, and maintained even after the detraining period, was associated with reduced inflammatory profile in the left ventricle and adipose tissue of rats subjected to MI. These data encourage enhancing cardiovascular autonomic function as a therapeutic strategy for the treatment of inflammatory process triggered by MI. Sao Judas Tadeu Univ USJT, Human Movement Lab, BR-03166000 Sao Paulo, Brazil Fed Univ Sao Paulo UNIFESP, Nutr Physiol Discipline, Dept Physiol, BR-04021001 Sao Paulo, Brazil Univ Extremo Catarinense UNESC, Lab Exercise Physiol & Biochem, BR-88806000 Criciuma, SC, Brazil Univ Sao Paulo, Sch Med, Heart Inst InCor, Hypertens Unit, BR-05403900 Sao Paulo, Brazil Univ Sao Paulo State UNESP, Dept Phys Educ, Immunometab Res Grp, BR-19060900 Presidente Prudente, SP, Brazil Univ Sao Paulo State UNESP, Dept Phys Educ, Immunometab Res Grp, BR-19060900 Presidente Prudente, SP, Brazil FAPESP: 13/14788-9 FAPESP: 07/58942-0 CNPq: CNPq: 563961/2010-4 CNPq: 479076/2012-0 CNPq: 457581/2013-1 CAPES: CAPES: 074/2012 CAPES: 095/2010

article i nfo Polyphenols consumption detected in red wine and grape juice may prevent or help in the treatment of hypertension. However, cardiovascular autonomic effects of polyphenols were poorly studied. Therefore, we evaluated the effects of resveratrol and grape juice treatments in hemodynamics, baroreflex sensitiv- ity, heart rate (HR) and blood pressure (BP) variability and cardiac redox parameters. Male Wistar rats were divided in 3 groups (n = 7/each) and treated for 30 days: only L-NAME-treated (60 mg/kg/day by oral gavage), L-NAME + resveratrol (L-NAME + R) and L-NAME + grape juice (L-NAME + G). BP signal was directly recorded and pulse interval (PI) and systolic arterial pressure (SAP) variability were analyzed in time and frequency domains. Baroreflex sensitivity (BRS) was determined by the alpha index. Oxidized and reduced glutathione concentrations were determined in cardiac tissue. L-NAME increased BP with no differences among groups (mean BP: L-NAME = 124 ± 4, L-NAME + R = 126 ± 3 and L-NAME + G = 125 ± 4 mmHg). PI and SAP variability expressed by total variance were also similar among groups. However, normalized low frequency (LF) and high frequency (HF) components of PI variability were lower and higher, respectively, in both R and G-treated groups when compared to only L-NAME group. In- terestingly, sympathetic modulation to the vessels (LF from SAP variability) and BRS were decreased and increased, respectively, only in L-NAME + R rats. Additionally, GSH/GSSG ratios were higher in L-NAME + R and L-NAME + G than in L-NAME group. Our results indicate that resveratrol and grape juice treatments can modulate autonomic function and promote cardiac redox benefits even when nitric oxide is decreased. Moreover, resveratrol influences not only cardiac but also vascular autonomic modulation.

Summary In the present study we evaluated the effects of short-term pyridostigmine bromide (0.14 mg/mL) treatment started early after myocardial infarction (MI) on left ventricular (LV) and autonomic functions in rats. Male Wistar rats were divided into control, pyridostigmine, infarcted and infarcted + pyridostigmine-treated groups. Pyridostigmine was administered in the drinking water, starting immediately after MI or sham operation, for 11 days. Left ventricular function was evaluated indirectly by echocardiography and directly by LV catheterization. Cardiovascular autonomic control was evaluated by baroreflex sensitivity (BRS), heart rate variability (HRV) and pharmacological blockade. All evaluations started after 7 days pyridostigmine treatment and were finalized after 11 days treatment. Pyridostigmine prevented the impairment of +dP/dT and reduced the MI area in infarcted + pyridostigmine compared with infarcted rats (7 ± 3% vs 17 ± 4%, respectively). Mean blood pressure was restored in infarcted + pyridostigmine compared with infarcted rats (103 ± 3 vs 94 ± 3 mmHg, respectively). In addition, compared with the infarcted group, pyridostigmine improved BRS, as evaluated by tachycardic (1.6 ± 0.2 vs 2.5 ± 0.2 b.p.m./mmHg, respectively) and bradycardic (−0.42 ± 0.01 vs −1.9 ± 0.1 b.p.m./mmHg) responses, and reduced the low frequency/high frequency ratio of HRV (0.81 ± 0.11 vs 0.24 ± 0.14, respectively). These improvements are probably associated with increased vagal tone and reduced sympathetic tone in infarcted + pyridostigmine compared with infarcted rats. In conclusion, the data suggest that short-term pyridostigmine treatment started early after MI can improve BRS, HRV and parasympathetic and sympathetic tone in experimental rats. These data may have potential clinical implications because autonomic markers have prognostic significance after MI.

Aims We evaluated autonomic and hemodynamic parameters and maximal oxygen consumption (VO 2 max) as possible determinants of mortality in streptozotocin (STZ) diabetic rats after myocardial infarction (MI). Method Male Wistar rats were divided into (n=8 of each): control sham (CS), diabetes sham (DS), MI (I), and diabetes+MI (DI). MI was induced 15days after STZ induction. VO 2 max was measured at 3 (basal), 30, 60, and 91 days after MI. Hemodynamic and autonomic parameters were evaluated 92days after MI. Results MI area was similar in infarcted groups (~44%). Mortality rate increased in the DI (70%) compared with I (53%) group. Cardiopulmonary baroreflex, sympathetic (48%) and vagal (33%) tonus, low frequency (LF) band (57%), and LF/high frequency (HF) band ratio (53%) were reduced in DI compared with I animals. Furthermore, cardiac output (CO), peripheral vascular resistance (PVR) impairment, and VO 2 max reductions were observed in the DI compared with the I group. Conclusions Our data suggest that the CO and PVR changes as well as VO 2 max reduction were probably associated with additional cardiac autonomic control impairment, and, consequently, increased mortality rate in diabetic rats after a chronic myocardial infarction.

The risks of chronic diseases associated with the increasing consumption of fructose-laden foods are amplified by the lack of regular physical activity and have become a serious public health issue worldwide. Moreover, childhood eating habits are strongly related to metabolic syndrome in adults. Thus, we aimed to investigate the preventive role of exercise training undertaken concurrently with a high fructose diet on cardiac function, hemodynamics, cardiovascular autonomic modulation and oxidative stress in male rats after weaning. Male Wistar rats were divided into 4 groups (n = 8/group): Sedentary control (SC), Trained control (TC), Sedentary Fructose (SF) and Trained Fructose (TF). Training was performed on a treadmill (8 weeks, 40-60% of maximum exercise test). Evaluations of cardiac function, hemodynamics, cardiovascular autonomic modulation and oxidative stress in plasma and in left ventricle (LV) were performed. Chronic fructose overload induced glucose intolerance and an increase in white adipose tissue (WAT) weight, in myocardial performance index (MPI) (SF:0.42±0.04 vs. SC:0.24±0.05) and in arterial pressure (SF:122±3 vs. SC:113±1 mmHg) associated with increased cardiac and vascular sympathetic modulation. Fructose also induced unfavorable changes in oxidative stress profile (plasmatic protein oxidation- SF:3.30±0.09 vs. SC:1.45±0.08 nmol/mg prot; and LV total antioxidant capacity (TRAP)-SF: 2.5±0.5 vs. SC:12.7±1.7 uM trolox). The TF group showed reduced WAT, glucose intolerance, MPI (0.35±0.04), arterial pressure (118±2mmHg), sympathetic modulation, plasmatic protein oxidation and increased TRAP when compared to SF group. Therefore, our findings indicate that cardiometabolic dysfunctions induced by fructose overload early in life may be prevented by moderate aerobic exercise training. Fil: Farah, Daniela. Universidade Presbiteriana Mackenzie; Brasil. Hospital Das Clinicas. Instituto Do Coracao; Brasil Fil: Nunes, Jonas. Universidade Presbiteriana Mackenzie; Brasil Fil: Sartori, Michelle. Universidade Nove de Julho; Brasil. Hospital Das Clinicas. Instituto Do Coracao; Brasil Fil: Da Silva Dias, Danielle. Universidade Nove de Julho; Brasil Fil: Sirvente, Raquel. Hospital Das Clinicas. Instituto Do Coracao; Brasil Fil: Silva, Maikon B.. Hospital Das Clinicas. Instituto Do Coracao; Brasil Fil: Fiorino, Patrícia. Universidade Presbiteriana Mackenzie; Brasil Fil: Morris, Mariana. Nova Southeastern University; Estados Unidos Fil: Llesuy, Susana Francisca. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina Fil: Farah, Vera. Universidade Presbiteriana Mackenzie; Brasil Fil: Irigoyen, Maria Cláudia. Hospital Das Clinicas. Instituto Do Coracao; Brasil Fil: De Angelis, Kátia. Universidade Nove de Julho; Brasil

CONTEXT AND OBJECTIVE: This study aimed to evaluate different mathematical post-analysis methods of determining lactate threshold in highly and lowly trained endurance runners. DESIGN AND SETTING: Experimental laboratory study, in a tertiary-level public university hospital. METHOD: Twenty-seven male endurance runners were divided into two training load groups: lowly trained (frequency < 4 times per week, < 6 consecutive months, training velocity ≥ 5.0 min/km) and highly trained (frequency ≥ 4 times per week, ≥ 6 consecutive months, training velocity < 5.0 min/km). The subjects performed an incremental treadmill protocol, with 1 km/h increases at each subsequent 4-minute stage. Fingerprint blood-lactate analysis was performed at the end of each stage. The lactate threshold (i.e. the running velocity at which blood lactate levels began to exponentially increase) was measured using three different methods: increase in blood lactate of 1 mmol/l at stages (DT1), absolute 4 mmol/l blood lactate concentration (4 mmol), and the semi-log method (semi-log). ANOVA was used to compare different lactate threshold methods and training groups. RESULTS: Highly trained athletes showed significantly greater lactate thresholds than lowly trained runners, regardless of the calculation method used. When all the subject data were combined, DT1 and semi-log were not different, while 4 mmol was significantly lower than the other two methods. These same trends were observed when comparing lactate threshold methods in the lowly trained group. However, 4 mmol was only significantly lower than DT1 in the highly trained group. CONCLUSION: The 4 mmol protocol did not show lactate threshold measurements comparable with DT1 and semi-log protocols among lowly trained athletes. RESUMO CONTEXTO E OBJETIVO: O objetivo do presente estudo é avaliar modelos matemáticos de pós-análise do limiar de lactato em grupos de corredores de longa distância muito ou pouco treinados. TIPO DE ESTUDO E LOCAL: Estudo laboratorial experimental. Hospital Público Universitário Terciário. MÉTODO: Vinte e sete corredores homens foram divididos em: pouco treinados (frequência < 4 vezes por semana, < 6 meses, velocidade ≥ 5,0 minutos/km) e muito treinados (frequência ≥ 4 vezes por semana, ≥ 6 meses, velocidade < 5,0 minutos/km). Os participantes foram submetidos a protocolo de esteira escalonado (1% inclinação) = 1 km/h por fase (4 minutos). Ao fim de cada estágio, análise da "impressão digital" metabolômica foi realizada. O limiar do lactato (i.e. velocidade em que o lactato sanguíneo aumenta exponencialmente) foi medido utilizando-se três métodos: aumento de 1 mmol/l da concentração, concentração absoluta de 4 mmol e método semi-log. ANOVA foi utilizada para comparar os diferentes limiares de lactato e grupos. RESULTADO: Atletas muito treinados apresentaram limiares de lactato maiores que os corredores pouco treinados, independentemente do método de cálculo utilizado. Comparando todos os corredores juntos, as análises de aumento de 1 mmol/l e semi-log não foram diferentes, enquanto a concentração absoluta de 4 mmol/l foi significativamente mais baixa que as dos dois outros métodos. Essas mesmas tendências foram observadas ao se compararem os métodos de limiar de lactato no grupo menos treinado. Entretanto, a análise absoluta de 4 mmol/l foi menor do que a do aumento de 1 mmol/l no grupo muito treinado. CONCLUSÃO: O método concentração absoluta de 4 mmol não mostrou mensurações comparáveis de limiar do lactato quando comparado com os protocolos aumento de 1 mmol/l e semi-log nos atletas pouco treinados.

Introduction: The angiotensin-converting enzyme 2 (ACE2)/angiotensin (Ang)-(1–7)/Mas axis could modulate the heart rate (HR) and blood pressure variabilities (BPV) which are important predictors of cardiovascular risk and provide information about the autonomic modulation of the cardiovascular system. Therefore we investigated the effect of Mas deficiency on autonomic modulation in wild type and Mas-knockout (KO) mice. Methods: Blood pressure was recorded at high sample rate (4000 Hz). Stationary sequences of 200–250 beats were randomly chosen. Frequency domain analysis of HR and BPV was performed with an autoregressive algorithm on the pulse interval sequences and on respective systolic sequences. Results: The KO group presented an increase of systolic arterial pressure (SAP; 127.26±11.20 vs 135.07±6.98 mmHg), BPV (3.54±1.54 vs 5.87±2.12 mmHg2), and low-frequency component of systolic BPV (0.12±0.11 vs 0.47±0.34 mmHg2). Conclusions: The deletion of Mas receptor is associated with an increase of SAP and with an increased BPV, indicating alterations in autonomic control. Increase of sympathetic vascular modulation in absence of Mas evidences the important role of Ang-(1–7)/Mas on cardiovascular regulation. Moreover, the absence of significant changes in HR and HRV can indicate an adaptation of autonomic cardiac balance. Our results suggest that the Ang-(1–7)/Mas axis seems more important in autonomic modulation of arterial pressure than HR.

We evaluated the effects of aerobic and resistance exercise training on ventricular morphometry and function, physical capacity, autonomic function, as well as on ventricular inflammatory status in trained rats prior to myocardial infarction. Male Wistar rats were divided into the following groups: sedentary+Sham, sedentary+myocardial infarction, aerobic trained+myocardial infarction, and resistance trained+myocardial infarction. Sham and myocardial infarction were performed after training periods. In the days following the surgeries, evaluations were performed. Aerobic training prevents aerobic (to a greater extent) and resistance capacity impairments, ventricular dysfunction, baroreflex sensitivity and autonomic disorders (vagal tonus decrease and sympathetic tonus increase) triggered by myocardial infarction. Resistance training was able to prevent negative changes to aerobic and resistance capacity (to a greater extent) but not to ventricular dysfunction, and it prevented cardiovascular sympathetic increments. Additionally, both types of training reduced left ventricle inflammatory cytokine concentration. Our results suggest that aerobic and, for the first time, dynamic resistance training were able to reduce sympathetic tonus to the heart and vessels, as well as preventing the increase in pro-inflammatory cytokine concentrations in the left ventricle of trained groups. These data emphasizes the positive effects of aerobic and dynamic resistance training on the prevention of the negative changes triggered by myocardial infarction.

We tested the hypothesis that an increase in the anti-inflammatory cholinergic pathway, when induced by pyridostigmine (PY), may modulate subtypes of lymphocytes (CD4+, CD8+, FOXP3+) and macrophages (M1/M2) soon after myocardial infarction (MI) in rats. Wistar rats, randomly allocated to receive PY (40 mg·kg−1·day−1) in drinking water or to stay without treatment, were followed for 4 days and then were subjected to ligation of the left coronary artery. The groups—denominated as the pyridostigmine-treated infarcted (IP) and infarcted control (I) groups—were submitted to euthanasia 3 days after MI; the heart was removed for immunohistochemistry, and the peripheral blood and spleen were collected for flow cytometry analysis. Noninfarcted and untreated rats were used as controls (C Group). Echocardiographic measurements were registered on the second day after MI, and heart rate variability was measured on the third day after MI. The infarcted groups had similar MI areas, degrees of systolic dysfunction, blood pressures, and heart rates. Compared with the I Group, the IP Group showed a significant higher parasympathetic modulation and a lower sympathetic modulation, which were associated with a small, but significant, increase in diastolic function. The IP Group showed a significant increase in M2 macrophages and FOXP3+ cells in the infarcted and peri-infarcted areas, a significantly higher frequency of circulating Treg cells (CD4+CD25+FOXP3+), and a less extreme decrease in conventional T cells (CD25+FOXP3−) compared with the I Group. Therefore, increasing cholinergic modulation with PY induces greater anti-inflammatory cell recruitment soon after MY in rats.

Fundacao de Amparo a Pesquisa do Estado de Sao Paulo National Counsel of Technological and Scientific Development (CNPq) Mackenzie University Coordination for the Improvement of Higher Education Personnel (CAPES) CAPES/FIPSE program Metabolic syndrome (MS) increases the risk of type 2 diabetes and cardiovascular disease. High consumption of fructose is a proposed cause of increased MS, manifested through hypertension, obesity, insulin resistance, and dyslipidemia. High NaCl also increases the risk of CD. The purpose of this study is to evaluate the influence of fructose and sodium on autonomic dysfunction and its relation with CD in MS. Fructose overload was started at weaning and continued through adulthood. Male Wistar rats (21 days) were divided into four groups: Control (C), fructose consumption (10 %, F), NaCl consumption (salt 1 % for the 10 last days, S), and fructose and NaCl (FS), and monitored for 8 weeks. Metabolic evaluations consisted of Lee index, glycemia, insulin and glucose tolerance tests, triglycerides, and total cholesterol measurements. Cardiovascular parameters measured were arterial pressure (AP) and cardiac function performed by echocardiography. They also measured the influence of renin angiotensin (RAS) and autonomic nervous systems by drug blockage with losartan, atropine, and atenolol. Energy analysis showed no change between groups. Fructose overload induced a MS state, confirmed by insulin resistance, glucose intolerance, and dyslipidemia. Fasting glucose was increased in F and FS rat groups compared with C and S groups. AP was higher in F, S, and FS groups in comparison with the C group. The hypotensive response after sympathetic blockade was increased in F, S, and FS versus C. The cardiac vagal tonus was reduced in F and FS animal groups. The intrinsic heart rate was decreased in the FS group (372 +/- A 9 bpm) compared with the C group (410 +/- A 13 bpm). The morphometric measurements evaluated through left ventricular diameter during diastole and the left ventricular diameter during systole decreased in the FS group (16 and 26 %, respectively). Diastolic function was reduced in F and FS. The depressor response induced by losartan was increased in the F group in comparison with other groups. However, there was a uniform increase in plasma ACE activity in all treated groups compared with the C group. Data suggest that early exposure to high fructose intake produced marked alterations in metabolic and cardiovascular function. When stimulated by NaCl, the fructose-fed subjects showed further impairment in cardiac function. Univ Fed Sao Paulo, Dept Med, Translat Med Div, Sao Paulo, SP, Brazil Univ Prebiteriana Mackenzie, Hlth & Biol Sci Ctr, Renal Cardiovasc & Metab Physiopharmacol Lab, Rua Consolacao 930, BR-01302907 Sao Paulo, SP, Brazil Univ Sao Paulo FMUSP, Hypertens Unit, Heart Inst InCor, Sch Med, Ave Doutor Eneas de Carvalho Aguiar 44, BR-05403900 Sao Paulo, SP, Brazil Fed Univ Maranhao UFMA, Sao Luis, MA, Brazil Univ Nove Julho UNINOVE, Translat Physiol Lab, Rua Vergueiro 235-249, BR-01504001 Sao Paulo, SP, Brazil Nova SE Univ, Coll Osteopath Med, 3200 South Univ Dr, Ft Lauderdale, FL 33328 USA Univ Fed Sao Paulo, Dept Med, Translat Med Div, Sao Paulo, SP, Brazil FAPESP: 2009/52556-7 Web of Science

OBJECTIVE: High fructose consumption contributes to the incidence of metabolic syndrome and, consequently, to cardiovascular outcomes. We investigated whether exercise training prevents high fructose diet-induced metabolic and cardiac morphofunctional alterations. METHODS: Wistar rats receiving fructose overload (F) in drinking water (100 g/l) were concomitantly trained on a treadmill (FT) for 10 weeks or kept sedentary. These rats were compared with a control group (C). Obesity was evaluated by the Lee index, and glycemia and insulin tolerance tests constituted the metabolic evaluation. Blood pressure was measured directly (Windaq, 2 kHz), and echocardiography was performed to determine left ventricular morphology and function. Statistical significance was determined by one-way ANOVA, with significance set at p

The aim of this study was to investigate metabolic and cardiovascular responses to walking in fructose-fed rats. Male Wistar rats were divided into control (C), sedentary fructose (SF) and walking fructose (WF). Fructose-fed rats received D-fructose (100 g/l). WF rats walked on a treadmill at constant load (0.3 km/h) during 1 h/day, 5 days/week for 8 weeks. Measurements of triglyceride concentrations, adipose tissue and glycemia were carried out together with insulin tolerance test to evaluate metabolic profile. Arterial pressure (AP) signals were directly recorded. Baroreflex sensitivity (BR) was evaluated by the reflex tachycardia (TR) and bradycardia (BR) to AP changes. The results showed that walking decreased the adipose tissue (SF: 6.5 ± 0.4; WF: 2.8 ± 0.1; C: 3.0 ± 0.3 g), blood triglyceride levels (SF: 291 ± 6.5; WF: 150 ± 8.1; C: 103 ± 4.5 mg/dl) and increased insulin sensitivity (SF: 2.5 ± 0.2; WF: 3.3 ± 0.32; C: 4.8 ± 0.4 %/min). Baroreflex sensitivity was improved in the WF group expressed by BR (SF: 0.75 ± 0.10; WF: 1.18 ± 0.10; C: 1.5 ± 0.14 ms/mmHg) and TR (SF: 0.80 ± 0.12; WF: 1.21 ± 0.10; C: 1.35 ± 0.11 ms/mmHg), as well as when verified by the alpha index. Although the WF group showed decreased AP when compared with the SF group, the values still enhanced in relation to C rats (SF: 137 ± 2; WF: 129 ± 1; C: 115 ± 6 mmHg). Our findings allow a better understanding of the effects of walking, a low-intensity exercise training, on the hemodynamic and metabolic aspects of male rats with metabolic syndrome and indicate that walking seems to be particularly effective in treating metabolic disturbances in this model.

Consumption of high levels of fructose in humans and animals leads to metabolic and cardiovascular dysfunction. There are questions as to the role of the autonomic changes in the time course of fructose-induced dysfunction. C57/BL male mice were given tap water or fructose water (100 g/l) to drink for up to 2 mo. Groups were control (C), 15-day fructose (F15), and 60-day fructose (F60). Light-dark patterns of arterial pressure (AP) and heart rate (HR), and their respective variabilities were measured. Plasma glucose, lipids, insulin, leptin, resistin, adiponectin, and glucose tolerance were quantified. Fructose increased systolic AP (SAP) at 15 and 60 days during both light (F15: 123 ± 2 and F60: 118 ± 2 mmHg) and dark periods (F15: 136 ± 4 and F60: 136 ± 5 mmHg) compared with controls (light: 111 ± 2 and dark: 117 ± 2 mmHg). SAP variance (VAR) and the low-frequency component (LF) were increased in F15 (>60% and >80%) and F60 (>170% and >140%) compared with C. Cardiac sympatho-vagal balance was enhanced, while baroreflex function was attenuated in fructose groups. Metabolic parameters were unchanged in F15. However, F60 showed significant increases in plasma glucose (26%), cholesterol (44%), triglycerides (22%), insulin (95%), and leptin (63%), as well as glucose intolerance. LF of SAP was positively correlated with SAP. Plasma leptin was correlated with triglycerides, insulin, and glucose tolerance. Results show that increased sympathetic modulation of vessels and heart preceded metabolic dysfunction in fructose-consuming mice. Data suggest that changes in autonomic modulation may be an initiating mechanism underlying the cluster of symptoms associated with cardiometabolic disease.

CONTEXTUALIZACAO: O treinamento fisico (TF) e capaz de reduzir a pressao arterial (PA) e prevenir o declinio da capacidade funcional. Entretanto, pouco tem sido estudado sobre os efeitos de menores volumes de treinamento em idosos com hipertensao arterial (HA). OBJETIVOS: Investigar os efeitos de um programa de TF multicomponente (treinamento aerobico, forca, flexibilidade e equilibrio) na PA, aptidao fisica e capacidade funcional de idosos com HA. METODOS: Trinta e seis idosos com HA e tratamento clinico otimizado foram submetidos a um programa de exercicios fisicos multicomponente, com duas sessoes semanais de 60 minutos cada, durante 12 semanas, em uma Unidade Basica de Saude (UBS). RESULTADOS: Comparados aos valores antes do TF, observou-se reducao de 3,6% da PA sistolica (p

Activation of renin-angiotensin system has been linked to cardiovascular and autonomic dysfunctions in diabetes. Experiments were performed to investigate the effects of angiotensin-converting enzyme inhibitor (ACEI), enalapril, on cardiac and autonomic functions in diabetic rats. Diabetes was induced by streptozotocin (50 mg/kg), and rats were treated with enalapril (1 mg · kg(-1) · d(-1)). After 30 days, evaluations were performed in control, diabetic, and enalapril-treated groups. Cardiac function was evaluated by echocardiography and through cannulation of the left ventricle (at baseline and in response to volume overload). Heart rate and systolic blood pressure variabilities were evaluated in the time and frequency domains. Streptozotocin rats had left ventricular systolic and diastolic dysfunctions, expressed by reduced ejection fraction and increased isovolumic relaxation time. The ACEI prevented these changes, improved diastolic cardiac responses to volume overload and total power of heart rate variability, reduced the ACE1 activity and protein expression and cardiac angiotensin (Ang) II levels, and increased angiotensin-converting enzyme 2 activity, despite unchanged blood pressure. Correlations were obtained between Ang II content with systolic and diastolic functions and heart rate variability. These findings provide evidence that the low-dose ACEI prevents autonomic and cardiac dysfunctions induced by diabetes without changing blood pressure and associated with reduced cardiac Ang II and increased angiotensin-converting enzyme 2 activity.

The objective of the present study was to investigate the effects of an acute aerobic exercise on arterial pressure (AP), heart rate (HR), and baroreflex sensitivity (BRS) in STZ-induced diabetic rats. Male Wistar rats were divided into control (n=8) and diabetic (n=8) groups. AP, HR, and BRS, which were measured by tachycardic and bradycardic (BR) responses to AP changes, were evaluated at rest (R) and postexercise session (PE) on a treadmill. At rest, STZ diabetes induced AP and HR reductions, associated with BR impairment. Attenuation in resting diabetes-induced AP (R:103±2versus PE:111±3 mmHg) and HR (R:290±7versus PE:328±10 bpm) reductions and BR dysfunction (R:-0.70±0.06versus PE:-1.21±0.09 bpm/mmHg) was observed in the postexercise period. In conclusion, the hemodynamic and arterial baro-mediated control of circulation improvement in the postexercise period reinforces the role of exercise in the management of cardiovascular risk in diabetes.

High-fructose diet is known to produce cardiovascular and metabolic pathologies. The objective was to determine whether the timing of high fructose (10% liquid solution) intake affect the metabolic and cardiovascular outcomes. Male C57BL mice with radiotelemetric probes were divided into four groups: (1) 24 h water (control); (2) 24 h fructose (F24); (3) 12 h fructose during the light phase (F12L); (4) 12 h fructose during the dark phase (F12D). All fructose groups had higher fluid intake. Body weight was increased in mice on restricted access with no difference in total caloric intake. Fasting glycemia was higher in groups with restricted access. F24 mice showed a fructose-induced blood pressure increase during the dark period. Blood pressure circadian rhythms were absent in F12L mice. Results suggest that the timing of fructose intake is an important variable in the etiology of cardiovascular and metabolic pathologies produced by high fructose consumption.