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We present a 3D discrete-continuum model to simulate blood pressure in large microvascular tissues in the absence of known capillary network architecture. Our hybrid approach combines a 1D Poiseuille flow description for large, discrete arteriolar and venular networks coupled to a continuum-based Darcy model, point sources of flux, for transport in the capillary bed. We evaluate our hybrid approach using a vascular network imaged from the mouse brain medulla/pons using multi-fluorescence high-resolution episcopic microscopy (MF-HREM). We use the fully-resolved vascular network to predict the hydraulic conductivity of the capillary network and generate a fully-discrete pressure solution to benchmark against. Our results demonstrate that the discrete-continuum methodology is a computationally feasible and effective tool for predicting blood pressure in real-world microvascular tissues when capillary microvessels are poorly defined., (© 2024 The Authors. International Journal for Numerical Methods in Biomedical Engineering published by John Wiley & Sons Ltd.)

In sleep apnea, airway obstruction causes intermittent hypoxia (IH). In animal studies, IH-dependent hypertension is associated with loss of vasodilator hydrogen sulfide (H 2 S), and increased H 2 S activation of sympathetic nervous system (SNS) activity in the carotid body. We previously reported that inhibiting cystathionine γ-lyase (CSE) to prevent H 2 S synthesis augments vascular resistance in control rats. The goal of this study was to evaluate the contribution of IH-induced changes in CSE signaling to increased blood pressure and vascular resistance. We hypothesized that chronic IH exposure eliminates CSE regulation of blood pressure (BP) and vascular resistance. In rats instrumented with venous catheters, arterial telemeters, and flow probes on the main mesenteric artery, the CSE inhibitor dl-propargylglycine (PAG, 50 mg/kg/day i.v. for 5 days) increased BP in Sham rats but decreased BP in IH rats [in mmHg, Sham ( n = 11): 114 ± 4 to 131 ± 6; IH ( n = 8): 131 ± 8 to 115 ± 7 mmHg, P < 0.05]. PAG treatment increased mesenteric vascular resistance in Sham rats but decreased it in IH rats ( day 5 / day 1 : Sham: 1.50 ± 0.07; IH: 0.85 ± 0.19, P < 0.05). Administration of the ganglionic blocker hexamethonium (to evaluate SNS activity) decreased mesenteric resistance in PAG-treated Sham rats more than in saline-treated Sham rats or PAG-treated IH rats. CSE immunoreactivity in IH carotid bodies compared with those from Sham rats. However, CSE staining in small mesenteric arteries was less in arteries from IH than in Sham rats but not different in larger arteries (inner diameter > 200 µm). These results suggest endogenous H 2 S regulates blood pressure and vascular resistance, but this control is lost after IH exposure with decreased CSE expression in resistance size arteries. IH exposure concurrently increases carotid body CSE expression and relative SNS control of blood pressure, suggesting both vascular and carotid body H 2 S generation contribute to blood pressure regulation. NEW & NOTEWORTHY These results suggest that CSE's protective role in the vasculature is impaired by simulated sleep apnea, which also upregulates CSE in the carotid body. Thus, this enzyme system can exert both pro- and antihypertensive effects and may contribute to elevated SNS outflow in sleep apnea.

Vasodilatory effects of insulin support the delivery of insulin and glucose to skeletal muscle. Concurrently, insulin exerts central effects that increase sympathetic nervous system activity (SNA), which is required for the acute maintenance of blood pressure (BP). Indeed, in a cohort of young healthy adults, herein we show that intravenous infusion of insulin increases muscle SNA while BP is maintained. We next tested the hypothesis that sympathoexcitation evoked by hyperinsulinemia restrains insulin-stimulated peripheral vasodilation and contributes to sustaining BP. To address this, a separate cohort of participants were subjected to 5-s pulses of neck suction (NS) to simulate carotid hypertension and elicit a reflex-mediated reduction in SNA. NS was conducted before and 60 min following intravenous infusion of insulin. Insulin infusion caused an increase in leg vascular conductance and cardiac output (CO; P < 0.050), with maintenance of BP ( P = 0.540). As expected, following NS, decreases in BP were greater in the presence of hyperinsulinemia compared with control ( P = 0.045). However, the effect of NS on leg vascular conductance did not differ between insulin and control conditions ( P = 0.898). Instead, the greater decreases in BP following NS in the setting of insulin infusion paralleled with greater decreases in CO ( P = 0.009). These findings support the idea that during hyperinsulinemia, SNA-mediated increase in CO, rather than restraint of leg vascular conductance, is the principal contributor to the maintenance of BP. Demonstration in isolated arteries that insulin suppresses α-adrenergic vasoconstriction suggests that the observed lack of restraint of leg vascular conductance may be attributed to sympatholytic actions of insulin. NEW & NOTEWORTHY We examined the role of sympathetic activation in restraining vasodilatory responses to hyperinsulinemia and sustaining blood pressure in healthy adults. Data are reported from two separate experimental protocols in humans and one experimental protocol in isolated arteries from mice. Contrary to our hypothesis, the present findings support the idea that during hyperinsulinemia, a sympathetically mediated increase in cardiac output, rather than restraint of peripheral vasodilation, is the principal contributor to the maintenance of systemic blood pressure.

High dietary sodium intake is a risk factor for arterial hypertension; given that the ability to overcome sympathetically mediated vasoconstriction (functional sympatholysis) is attenuated in individuals with hypertension, we investigated the cardiovascular responses to high salt (HS) intake in healthy humans. We hypothesized that a HS intake of 15 g/day for 7 days would attenuate functional sympatholysis and augment the blood pressure response to handgrip exercise (HGE). Thirteen participants (6 males, 7 females) underwent 2 individual days of testing. Beat-by-beat blood pressure and heart rate were recorded throughout the trial on the non-exercising limb. Forearm blood flow was derived from ultrasonography on the brachial artery of the exercising limb. Participants then underwent a flow-mediated dilation (FMD) test. Next, a submaximal HGE was performed for 7 min with lower body negative pressure initiated during minutes 5-7. A single spot urine sample revealed a significant increase in sodium excretion during the HS conditions ( p < 0.01). FMD was reduced during the HS condition. Mean arterial pressure was significantly higher during HS intake. No alteration to functional sympatholysis was found between conditions ( p > 0.05). In summary, HS intake increases blood pressure without impacting functional sympatholysis or blood pressure responsiveness during HGE. These findings indicate that brachial artery dysfunction precedes an inefficient functional sympatholysis. Novelty Functional sympatholysis was not impacted by 1 week of high sodium intake. High sodium intake augmented the rate pressure product during handgrip exercise in healthy humans.

Dietary salt restriction is a well-established approach to lower blood pressure and reduce cardiovascular disease risk in hypertensive individuals. However, little is currently known regarding the effects of salt restriction on central and peripheral hemodynamic responses to exercise in those with hypertension. Therefore, this study sought to determine the impact of salt restriction on the central and peripheral hemodynamic responses to static-intermittent handgrip (HG) and dynamic single-leg knee extension (KE) exercise in individuals with hypertension. Twenty-two subjects (14 men and 8 women, 51 ± 10 yr, 173 ± 11 cm, 99 ± 23 kg) forewent their antihypertensive medication use for at least 2 wk before embarking on a 5-day liberal salt (LS: 200 mmol/day) diet followed by a 5-day restricted salt (RS: 10 mmol/day) diet. Subjects were studied at rest and during static intermittent HG exercise at 15, 30, and 45% of maximal voluntary contraction and KE exercise at 40, 60, and 80% of maximum KE work rate. Salt restriction lowered resting systolic blood pressure (supine: -12 ± 12 mmHg, seated: -17 ± 12 mmHg) and diastolic blood pressure (supine: -3 ± 9 mmHg, seated: -5 ± 7 mmHg, P < 0.05). Despite an ~8 mmHg lower mean arterial blood pressure during both HG and KE exercise following salt restriction, neither central nor peripheral hemodynamics were altered. Therefore, salt restriction can lower blood pressure during exercise in subjects with hypertension, reducing the risk of cardiovascular events, without impacting central and peripheral hemodynamics during either arm or leg exercise. NEW & NOTEWORTHY This is the first study to examine the potential blood pressure-lowering benefit of a salt-restrictive diet in individuals with hypertension without any deleterious effects of exercising blood flow. While mean arterial pressure decreased by ~8 mmHg following salt restriction, these findings provide evidence for salt restriction to provide protective effects of reducing blood pressure without inhibiting central or peripheral hemodynamics required to sustain arm or leg exercise in subjects with hypertension.

Based primarily on the rational that adequate diastolic pressure is needed to maintain sufficient coronary blood for myocardial needs, diastolic pressure has been proposed as a treatment target for patients in shock. To date, clinical evidence supporting this is limited to observational data. Key points are that what is important for tissues is flow not pressure; the coronary circulation has very large flow reserves and can maintain flow with a low pressure; raising arterial pressure by only increasing vascular resistance does not alter tissue perfusion and could even increase myocardial oxygen demand. Targeting diastolic pressure can lead to over use of vasopressors, which studies have associated with worse outcome. Pressor management in shock should include assessment of indicators of tissue perfusion and changes in flow if possible., (Copyright © 2018. Published by Elsevier Inc.)

Background: Given the anxiety patients experience during angiography, evidence supporting the efficacy of music therapy during these angiographic procedures is potentially of clinical value., Objective: To analyze the existing literature forthe use of music therapy during cerebral, coronary, and peripheral angiography to determine whether it improves patient anxiety levels, heart rate, and blood pressure during the procedure., Methods: PubMed, Embase, and Scopus were searched to identify studies of interest. Inclusion criteria included studies reporting using music therapy in either cerebral, coronary, or peripheral angiography. Studies focused on a pediatric population; animal studies and case reports were excluded. Participant demographics, interventions, and outcomes were collected by two study authors. Bias and study quality of randomized controlled trials (RCTs) were assessed using the Cochrane Risk of Bias Tool. Separate meta-analyses of the RCTs were performed to compare State Trait Anxiety Inventory (STAI), heart rate (HR), and systolic and diastolic blood pressure (SBP and DBP) in the music intervention group versus control group. Heterogeneity was determined by calculating I 2 values, and a random-effects model was used when heterogeneity exceeded 50%., Results: The preprocedure to postprocedure improvement in STAI was significantly greater in the experimental group than the control group (p=0.004), while the decrease in HR, SBP, and DBP was not significant., Conclusions: Recorded music and/or music therapy in angiography significantly decreases patients' anxiety levels, while it has little to no effect on HR and BP. This meta-analysis is limited by the relatively few RCTs published on this subject., Prospero Registration Number: CRD42018099103., Competing Interests: Competing interests: CPK: (1) director of CME course titled ’Endoscopic minimally invasive intracerebral hemorrhage evacuation' funded by Penumbra and (2) recipient of a Siemens Foundation research grant. JB: son of Arani Bose, MD, Chief Medical Officer and Chairman of Penumbra, Inc. JM: National/International PI/Co-PI: INVEST (Co-PI), COMPASS (Co-PI), THERAPY (PI), FEAT (PI), POSITIVE (Co-PI), BARREL (PI); consultant: TSP, Rebound Therapeutics, Viseon, Pulsar, Cerebrotech, Endostream, Vastrax; Investor/Stockholder/Owner: Cerebrotech, TSP, Endostream, Apama, Rebound, Viseon, Neurvana, Cardinal Consulting, BlinkTBI, Serenity, NTI., (© Author(s) (or their employer(s)) 2019. No commercial re-use. See rights and permissions. Published by BMJ.)

The effect of traumatic spinal cord injury (TSCI) on spinal cord blood flow (SCBF) in humans is unknown. Whether intervention to achieve the recommended mean arterial pressure (MAP) guideline of 85-90 mm Hg improves SCBF is also unclear. Here, we use laser speckle contrast imaging intraoperatively to visualize blood flow at the injury site in 22 patients with acute, severe spinal cord injuries (American Spinal Injuries Association Impairment Scale, grades A-C). In 17 of 22 patients, injury-site metabolism was also monitored with a microdialysis catheter placed intradurally on the surface of the injured cord. We observed three different SCBF patterns, characterized by distinct injury-site metabolic signatures, which we term necrosis-penumbra, hyperperfusion, and patchy-perfusion. The necrosis-penumbra pattern, only observed in thoracic injuries, had a core of low blood flow (necrosis) with regions of intermediate blood flow on either side (penumbra). The hyperperfusion pattern, only observed in cervical injuries, had very high blood flow throughout the injury site. The patchy-perfusion pattern, found in cervical and thoracic injuries, had irregular regions of low, intermediate, and high blood flow. Though intervention to increase MAP by 20 mm Hg increased overall blood flow at the injury site, in 5 of 22 patients, blood flow increased in some regions, but, surprisingly, decreased in other regions. We term this phenomenon blood pressure-induced local steal. In 7 of 19 patients with MAP 85-90 mm Hg, parts of the injury site were only perfused in systole, but not in diastole, which we term diastolic ischemia. We conclude that acute, severe TSCI produces three pathological blood flow patterns at the injury site. Intervention to increase blood pressure may elicit potentially detrimental SCBF responses in some patients.

It is proposed that, at very low loads, greater blood flow restriction (BFR) pressures might be required for muscular adaptation to occur. The cardiovascular and hyperemic response to very low loads combined with relative levels of BFR is unknown. Ninety-seven participants were recruited and assigned to 1 of 4 exercise conditions: 15% of 1-repetition maximum (1RM) without BFR (15/00), 15% 1RM with BFR at 40% of arterial occlusion pressure (AOP) (15/40), 15% of 1RM with BFR at 80% of AOP (15/80), and 70% of 1RM without BFR (70/00). Participants performed 4 sets of unilateral biceps curls. Blood pressure was measured before and after exercise; brachial artery blood flow was measured before exercise, following the second set, and 1 min following exercise. Systolic blood pressure increased following exercise in all conditions (+10 (11) mm Hg, P < 0.0005). Diastolic pressure increased in all but 70/00 (+2 (11) mm Hg, P = 0.107). Brachial artery blood flow increased following the second set of exercise in all but 15/80 (+43.4 (76.8) mL·min -1 , P = 0.348). One minute following exercise and cuff deflation, there were no differences in blood flow between conditions (P > 0.05). Similarly, artery diameter was increased in all conditions except 15/80 (+0.002 (0.041) cm, P = 0.853) following the second set, and increased in all conditions by 1 min following exercise (P < 0.05). In conclusion, exercise-induced hyperemia is blunted with increasing pressures of BFR. There is a modest increase in blood pressure at very low loads of resistance exercise in the upper body.

Purpose: Vascular dysfunction and ischemia are believed to play an important part in the pathogenesis of glaucoma and especially of normal tension glaucoma (NTG). The aim of the present study was to analyze the blood pressure (BP) and heart rate variability patterns in patients with primary open-angle glaucoma (POAG) and NTG compared with controls., Methods: In total, 37 patients with POAG, 27 patients with NTG, and 82 control subjects were included in a prospective clinical validation study. Continuous BP and heart rate were simultaneously recorded over 30 min (Glaucoscreen, aviant GmbH, Jena, Germany) under resting conditions. Time series of heart rate, systolic blood pressure (SBP) and diastolic blood pressure (DBP) were extracted and analyzed calculating univariate linear (time domain, frequency domain), nonlinear (symbolic dynamics), and bivariate (joint symbolic dynamics) indices., Results: Overall, 12 parameters could be identified that were significantly different when comparing POAG patients and controls, whereas 80 parameters were significantly different in NTG patients compared with controls. The optimum set consisting of three indices showed a sensitivity of 81.5% at a specificity of 86.6% for NTG patients compared with a sensitivity of 62.2% at a specificity of 82.9% for POAG patients., Conclusions: Alterations in BP variability and coupling with heart rate suggest impaired patterns of autonomic cardiovascular regulation in glaucoma patients especially in patients with NTG.

Measurement of arterial pressure is one of the most basic elements of patient management. Arterial pressure is determined by the volume ejected by the heart into the arteries, the elastance of the walls of the arteries, and the rate at which the blood flows out of the arteries. This review will discuss the three forces that determine the pressure in a vessel: elastic, kinetic, and gravitational energy. Emphasis will be placed on the importance of the distribution of arterial resistances, the elastance of the walls of the large vessels, and critical closing pressures in small arteries and arterioles. Regulation of arterial pressure occurs through changes in cardiac output and changes in vascular resistance, but these two controlled variables can sometimes be in conflict.

A fluid dynamic study of blood flow within the umbilical vessels of the human maternal-fetal circulatory system is considered. It is found that the umbilical coiling index (UCI) is unable to distinguish between cords of significantly varying pressure and flow characteristics, which are typically determined by the vessel curvature, torsion and length. Larger scale geometric non-uniformities superposed over the inherent coiling, including cords exhibiting width and/or local UCI variations as well as loose true knots, typically produce a small effect on the total pressure drop. Crucially, this implies that a helical geometry of mean coiling may be used to determine the steady vessel pressure drop through a more complex cord. The presence of vessel constriction, however, drastically increases the steady pressure drop and alters the flow profile. For pulsatile-flow within the arteries, the steady pressure approximates the time-averaged value with high accuracy over a wide range of cords. Furthermore, the relative peak systolic pressure measured over the period is virtually constant and approximately 25% below the equivalent straight-pipe value for a large range of non-straight vessels. Interestingly, this suggests that the presence of vessel helicity dampens extreme pressures within the arterial cycle and may provide another possible evolutionary benefit to the coiled structure of the cord., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Purpose: This study investigated whether reported improvements in blood flow distribution, and the possible related effects on thermoregulation during exercise following supplementation with beetroot juice (BR), a rich source of dietary nitrate (NO 3 - ), are mitigated in the heat., Methods: 12 male endurance-trained cyclists (age 27 ± 6 years, VO 2peak 68.6 ± 8.1 ml kg -1  min -1 ) completed two 60 min submaximal cycling trials at 60% of VO 2peak power output. Trials were performed in hot environmental conditions (33.3 ± 0.4 °C, 48.8 ± 3.0% RH) following 3 days of supplementation with either NO 3 - -rich BR (6.5 mmol NO 3 - for 2 days and 13 mmol NO 3 - ) were measured before and after the supplementation period. During exercise, cutaneous blood flow, blood pressure (MAP), core temperature (T 3 - -depleted placebo (PLA). Salivary NO 3 - and nitrite (NO 2 - ) were measured before and after the supplementation period. During exercise, cutaneous blood flow, blood pressure (MAP), core temperature (T c ), mean skin temperature (T sk ), indices of muscle oxygenation and oxygen (O 2 ) consumption were measured., Results: Salivary NO 3 - increased significantly following BR by 680 and 890%, respectively. There were no significant differences observed for cutaneous blood flow, MAP, T 2 - increased significantly following BR by 680 and 890%, respectively. There were no significant differences observed for cutaneous blood flow, MAP, T c , T sk , muscle oxygenation, or O 2 consumption between BR and PLA., Conclusion: This investigation shows that the ergogenic effects and health benefits of BR supplementation, such as augmented cutaneous blood flow, reduced MAP, increased muscle oxygenation, and improved aerobic efficiency may be attenuated when exercise is performed in hot conditions.

New Findings: What is the central question of this study? Stress-sensitive arterial hypertension is considered to be controlled by changes in central and peripheral sympathetic regulating mechanisms, which eventually result in haemodynamic alterations and blood pressure elevation. Therefore, study of the early stages of development of hypertension is of particular interest, because it helps in understanding the aetiology of the disease. What is the main finding and its importance? Non-invasive in vivo investigation in ISIAH rats demonstrated that establishment of sustainable stress-sensitive hypertension is accompanied by a decrease in prefrontal cortex activity and mobilization of hypothalamic processes, with considerable correlations between haemodynamic parameters and individual metabolite ratios. The study of early development of arterial hypertension in association with emotional stress is of great importance for better understanding of the aetiology and pathogenesis of the hypertensive disease. Magnetic resonance imaging (MRI) was applied to evaluate the changes in haemodynamics and brain metabolites in 1- and 3-month-old inherited stress-induced arterial hypertension (ISIAH) rats (10 male rats) with stress-sensitive arterial hypertension and in control normotensive Wistar Albino Glaxo (WAG) rats (eight male rats). In the 3-month-old ISIAH rats, the age-dependent increase in blood pressure was associated with increased blood flow through the renal arteries and decreased blood flow in the lower part of the abdominal aorta. The renal vascular resistance in the ISIAH rats decreased during ageing, although at both ages it remained higher than the renal vascular resistance in WAG rats. An integral metabolome portrait demonstrated that development of hypertension in the ISIAH rats was associated with an attenuation of the excitatory and energetic activity in the prefrontal cortex, whereas in the WAG rats the opposite age-dependent changes were observed. In contrast, in the hypothalamus of 3-month-old ISIAH rats, an increase in energetic activity and prevalence of excitatory over inhibitory neurotransmitters was noticed. The blood flow through the main arteries showed a positive correlation with glutamate and glutamine levels in the hypothalamus and a negative correlation with the hypothalamic GABA level. The blood pressure values were positively correlated with hypothalamic choline levels. Thus, the early development of stress-sensitive hypertension in the ISIAH rats is accompanied by considerable changes both in brain metabolite ratios and in the parameters of blood flow through the main arteries., (© 2017 Institute of Cytology and Genetics (SB RAS). Experimental Physiology © 2017 The Physiological Society.)

Background: Adjuvant cancer treatments have been shown to decrease cardiac function. In addition to changes in cardiovascular risk, there are several additional functional consequences including decreases in exercise capacity and increased incidence of cancer-related fatigue. However, the effects of adjuvant cancer treatment on peripheral vascular function during exercise in cancer survivors have not been well documented. We investigated the vascular responses to exercise in cancer survivors previously treated with adjuvant cancer therapies., Methods and Results: Peripheral vascular responses were investigated in 11 cancer survivors previously treated with adjuvant cancer therapies (age 58±6 years, 34±30 months from diagnosis) and 9 healthy controls group matched for age, sex, and maximal voluntary contraction. A dynamic handgrip exercise test at 20% maximal voluntary contraction was performed with simultaneous measurements of forearm blood flow and mean arterial pressure. Forearm vascular conductance was calculated from forearm blood flow and mean arterial pressure. Left ventricular ejection time index (LVETi) was derived from the arterial pressure wave form. Forearm blood flow was attenuated in cancer therapies compared to control at 20% maximal voluntary contraction (189.8±53.8 vs 247.9±80.3 mL·min -1 , respectively). Forearm vascular conductance was not different between groups at rest or during exercise. Mean arterial pressure response to exercise was attenuated in cancer therapies compared to controls (107.8±10.8 vs 119.2±16.2 mm Hg). LEVTi was lower in cancer therapies compared to controls., Conclusions: These data suggest an attenuated exercise blood flow response in cancer survivors ≈34 months following adjuvant cancer therapy that may be attributed to an attenuated increase in mean arterial pressure., (© 2017 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.)

Purpose: Previous work has shown nitric oxide (NO) contributes to ~15% of the hyperemic response to dynamic exercise in healthy humans. This NO-mediated vasodilation occurs, in part, via increases in intracellular cyclic guanosine monophosphate (cGMP), which is catabolized by phosphodiesterase. We sought to examine the effect of phosphodiesterase-5 (PDE-5) inhibition on forearm blood flow (FBF) responses to dynamic handgrip exercise in healthy humans and the role of NO. We hypothesized exercise hyperemia would be augmented by sildenafil citrate (SDF, PDE-5 inhibitor). We further hypothesized any effect of SDF on exercise hyperemia would be abolished with intra-arterial infusion of the NO synthase (NOS) inhibitor L-N G -monomethyl arginine (L-NMMA)., Methods: FBF (Doppler ultrasound) was assessed at rest and during 5 min of dynamic forearm handgrip exercise at 15% of maximal voluntary contraction under control (saline) conditions and during 3 experimental protocols: (1) oral SDF (n = 10), (2) intra-arterial L-NMMA (n = 20), (3) SDF and L-NMMA (n = 10). FBF responses to intra-arterial sodium nitroprusside (NTP, NO donor) were also assessed., Results: FBF increased with exercise (p < 0.01). Intra-arterial infusion of L-NMMA resulted in a reduction in exercise hyperemia (17 ± 1 to 15 ± 1 mL/dL/min, p < 0.01). Although the hyperemic response to NTP was augmented by SDF (area under the curve: 41 ± 7 vs 61 ± 11 AU, p < 0.01), there was no effect of SDF on exercise hyperemia (p = 0.33)., Conclusions: Despite improving NTP-mediated vasodilation, oral SDF failed to augment exercise hyperemia in young, healthy adults. These observations reflect a minor contribution of NO and the cGMP pathway during exercise hyperemia in healthy young humans.

Background: Despite concerns regarding hypoperfusion in patients with large-artery occlusive disease, strict blood pressure (BP) control has become adopted as a safe strategy for risk reduction of stroke. We examined the relationship between BP control, blood flow, and risk of subsequent stroke in the prospective Vertebrobasilar Flow Evaluation and Risk of Transient Ischemic Attack and Stroke (VERiTAS) study., Methods: The VERiTAS study enrolled patients with recent vertebrobasilar (VB) transient ischemic attack or stroke and ≥50% atherosclerotic stenosis or occlusion of vertebral or basilar arteries. Hemodynamic status was designated as low or normal based on quantitative magnetic resonance angiography. Patients underwent standard medical management and follow-up for primary outcome event of VB territory stroke. Mean BP during follow-up (<140/90 versus ≥140/90 mm Hg) and flow status were examined relative to subsequent stroke risk using Cox proportional hazards analysis., Results: The 72 subjects had an average of 3.8 ± 1.2 BP recordings over 20 ± 8 months of follow-up; 39 (54%) had mean BP of<140/90 mm Hg. The BP groups were largely comparable for baseline demographics, risk factors, and stenosis severity. Comparing subgroups stratified by BP and hemodynamic status, we found that patients with both low flow and BP <140/90 mm Hg (n = 10) had the highest risk of subsequent stroke, with hazard ratio of 4.5 (confidence interval 1.3-16.0, P = .02), compared with the other subgroups combined., Conclusions: Among a subgroup of patients with VB disease and low flow, strict BP control (BP <140/90) may increase the risk of subsequent stroke., (Copyright © 2017 National Stroke Association. Published by Elsevier Inc. All rights reserved.)

Physiological compensation to postural stress is weakened after long-duration water immersion (WI), thus predisposing individuals to orthostatic intolerance. This study was conducted to compare hemodynamic responses to postural stress following exposure to WI alone (Air WI), hyperbaric oxygen alone in a hyperbaric chamber (O 2 HC), and WI combined with hyperbaric oxygen (O 2 WI), all at a depth of 1.35 ATA, and to determine whether hyperbaric oxygen is protective of orthostatic tolerance. Thirty-two healthy men underwent up to 15 min of 70° head-up tilt (HUT) testing before and after a single 6-h resting exposure to Air WI ( N  = 10), O 2 HC ( N  = 12), or O 2 WI ( N  = 10). Heart rate (HR), blood pressure (BP), cardiac output (Q), stroke volume (SV), forearm blood flow (FBF), and systemic and forearm vascular resistance (SVR and FVR) were measured. Although all subjects completed HUT before Air WI, three subjects reached presyncope after Air WI exposure at 10.4, 9.4, and 6.9 min. HUT time did not change after O 2 WI or O 2 HC exposures. Compared to preexposure responses, HR increased (+10 and +17%) and systolic BP (-13 and -8%), and SV (-16 and -23%) decreased during HUT after Air WI and O 2 WI, respectively. In contrast, HR and SV did not change, and systolic (+5%) and diastolic BP (+10%) increased after O 2 HC Q decreased (-13 and -7%) and SVR increased (+12 and +20%) after O 2 WI and O 2 HC, respectively, whereas SVR decreased (-9%) after Air WI Opposite patterns were evident following Air WI and O 2 HC for FBF (-26 and +52%) and FVR (+28 and -30%). Therefore, breathing hyperbaric oxygen during WI may enhance post-WI cardiovascular compensatory responses to orthostatic stress., (© 2016 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.)

The cardiovascular responses to passive limb movement (PLM) at the knee are well established, however, responses to PLM at other joints involving smaller muscle volume are unknown. To compare the cardiovascular responses to passive movement at other joints, 10 participants underwent a PLM protocol in which the wrist, elbow, ankle, and knee joints were passively extended and flexed at 1 Hz for 1 min. Heart rate (HR), mean arterial blood pressure (MAP), and arterial blood flow to that limb segment (BF) were measured and vascular conductance (VC) was calculated for a 30-sec baseline period and for 3-sec intervals throughout PLM protocols. PLM of the knee and elbow resulted in significant increases in BF and VC from baseline values with peak values 180% (P < 0.001) greater than baseline. PLM of the elbow resulted in significant increases in BF and VC from baseline values with peak values 109% and 115% (P < 0.001) greater than baseline, respectively. No changes in BF and VC were observed in the ankle and wrist. Furthermore, the greater increase in blood flow per limb segment volume in the thigh and upper arm (62.8 ± 36.5 and 55.5 ± 30.3 mL min(-1) L(-1), respectively) compared to the forearm and lower leg (23.6 ± 16.7 and 19.1 ± 10.3 mL min(-1) L(-1), respectively) indicates the limb volume is not solely responsible for the differences in the hyperemic responses. These data indicate that the use of PLM to assess vascular function or as a rehabilitation modality to maintain vascular health may be most appropriate for the muscles that span the elbow and knee., (Published 2016. This article is a U.S. Government work and is in the public domain in the USA. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.)

Many studies showing a relation between low blood pressure (BP) and adverse health outcomes in older persons suggest that low BP gives rise to reduced cerebral blood flow (CBF). However, limited evidence is available about this association. Baseline data of 203 participants in the Discontinuation of Antihypertensive Treatment in the Elderly (DANTE) trial were used (mean age, 81 years, using antihypertensive medication and with mild cognitive deficits). BP, BP changes on standing, and CBF derived from pseudo-continuous arterial spin-labeling magnetic resonance imaging were assessed in all participants. In 102 participants who were randomly assigned to 4-month continuation (n=47) or discontinuation of antihypertensive treatment (n=55), BP and CBF change were evaluated at 4-month follow-up. Systolic and diastolic BP were not associated with CBF (B=-0.21, P=0.50 and B=-1.07, P=0.07), neither were mean arterial pressure, pulse pressure, and BP changes on standing. In subgroups of participants with small vessel-related cerebral pathologies, including high white matter hyperintensity volume, microbleeds, and lacunar infarcts, or in participants with lower cognition or diabetes mellitus, no association was found between any BP parameters and CBF. Furthermore, compared to the continuation group, CBF change at 4 months was not different in the discontinuation group (B=-0.12, P=0.23). Contrary to the notion that lower BP in old age is associated with decreased CBF, our data do not show this association in older persons using antihypertensive medication and with mild cognitive deficits. Also, this association was not present in subgroups of more vulnerable persons, reflected by small vessel-related cerebral pathologies, lower cognition, or diabetes mellitus., (© 2015 American Heart Association, Inc.)

In reduced-order (0D/1D) blood or respiratory flow models, pressure losses at junctions are usually neglected. However, these may become important where velocities are high and significant flow redirection occurs. Current methods for estimating losses rely on relatively complex empirical equations that are only valid for specific junction geometries and flow regimes. In pulsatile multi-directional flows, switching between empirical equations upon reversing flow may introduce unrealistic discontinuities in simulated haemodynamic waveforms. Drawing from work by Bassett et al. (SAE Trans 112:565-583, 2003), we therefore developed a unified method (Unified0D) for estimating loss coefficients that can be applied to any junction (i.e. any number of branches at any angle) and any flow regime. Discontinuities in simulated waveforms were avoided by extending Bassett et al.'s control volume-based method to incorporate a 'pseudodatum' supplier branch, an imaginary effective vessel containing all inflow to the junction. Energy exchange between diverging flow streams was also accounted for empirically. The formulation was validated using high resolution computational fluid dynamics in a wide range flow conditions and junction configurations. In a pulsatile 1D simulation exhibiting transitions between four different flow regimes, the new formulation produced smooth transitions in calculated pressure losses., (Copyright © 2015 John Wiley & Sons, Ltd.)

Purpose: To test the hypothesis that blood flow autoregulation in the optic nerve head has less reserve to maintain normal blood flow in the face of blood pressure-induced ocular perfusion pressure decrease than a similar magnitude intraocular pressure-induced ocular perfusion pressure decrease., Materials and Methods: Twelve normal non-human primates were anesthetized by continuous intravenous infusion of pentobarbital. Optic nerve blood flow was monitored by laser speckle flowgraphy. In the first group of animals (n = 6), the experimental eye intraocular pressure was maintained at 10 mmHg using a saline reservoir connected to the anterior chamber. The blood pressure was gradually reduced by a slow injection of pentobarbital. In the second group (n = 6), the intraocular pressure was slowly increased from 10 mmHg to 50 mmHg by raising the reservoir. In both experimental groups, optic nerve head blood flow was measured continuously. The blood pressure and intraocular pressure were simultaneously recorded in all experiments., Results: The optic nerve head blood flow showed significant difference between the two groups (p = 0.021, repeat measures analysis of variance). It declined significantly more in the blood pressure group compared to the intraocular pressure group when the ocular perfusion pressure was reduced to 35 mmHg (p < 0.045) and below. There was also a significant interaction between blood flow changes and the ocular perfusion pressure treatment (p = 0.004, adjusted Greenhouse & Geisser univariate test), indicating the gradually enlarged blood flow difference between the two groups was due to the ocular perfusion pressure decrease., Conclusions: The results show that optic nerve head blood flow is more susceptible to an ocular perfusion pressure decrease induced by lowering the blood pressure compared with that induced by increasing the intraocular pressure. This blood flow autoregulation capacity vulnerability to low blood pressure may provide experimental evidence related to the hemodynamic pathophysiology in glaucoma.

Recent work suggests that β-adrenergic vasodilation offsets α-adrenergic vasoconstriction in young women, but this effect is lost after menopause. Given these age-related vascular changes, we tested the hypothesis that older women would exhibit a greater change in vascular conductance following baroreflex perturbation compared with young women. In 10 young (21 ± 1 yr) and 10 older (62 ± 2 yr) women, mean arterial pressure (MAP; Finometer), heart rate (HR), cardiac output (CO; Modelflow), total vascular conductance (TVC), and leg vascular conductance (LVC, duplex-Doppler ultrasound) were continuously measured in response to 5-s pulses of neck suction (NS; -60 Torr) and neck pressure (NP; +40 Torr) to simulate carotid hypertension and hypotension, respectively. Following NS, decreases in MAP were similar between groups; however, MAP peak response latency was slower in older women (P < 0.05). Moreover, at the time of peak MAP, increases in LVC (young, -11.5 ± 3.9%LVC vs. older, +19.1 ± 7.0%LVC; P < 0.05) and TVC were greater in older women, whereas young women exhibited larger decreases in HR and CO (young, -10 ± 3% CO vs. older, +0.8 ± 2% CO; P < 0.05). Following NP, increases in MAP were blunted (young, +14 ± 1 mmHg vs. older, +8 ± 1 mmHg; P < 0.05) in older women, whereas MAP response latencies were similar. Interestingly, decreases in LVC and TVC were similar between groups, but HR and CO (young, +7.0 ± 2% CO vs. older, -4.0 ± 2% CO; P < 0.05) responses were attenuated in older women. These findings suggest that older women have greater reliance on vascular conductance to modulate MAP via carotid baroreflex, whereas young women rely more on cardiac responsiveness. Furthermore, older women demonstrate a blunted ability to increase MAP to hypotensive stimuli., (Copyright © 2014 the American Physiological Society.)

Clinical evidence indicates that obstructive sleep apnea is more common and more severe in men compared with women. Sex differences in the vasoconstrictor response to hypoxemia-induced sympathetic activation might contribute to this clinical observation. In the current laboratory study, we determined sex differences in the acute physiological responses to maximal voluntary end-expiratory apnea (MVEEA) during wakefulness in healthy young men and women (26 ± 1 yr) as well as healthy older men and women (64 ± 2 yr). Mean arterial pressure (MAP), heart rate (HR), brachial artery blood flow velocity (BBFV, Doppler ultrasound), and cutaneous vascular conductance (CVC, laser Doppler flowmetry) were measured, and changes in physiological parameters from baseline were compared between groups. The breath-hold duration and oxygen-saturation nadir were similar between groups. In response to MVEEA, young women had significantly less forearm vasoconstriction compared with young men (ΔBBFV: 2 ± 7 vs. -25 ± 6% and ΔCVC: -5 ± 4 vs. -31 ± 4%), whereas ΔMAP (12 ± 2 vs. 16 ± 3 mmHg) and ΔHR (4 ± 2 vs. 6 ± 3 bpm) were comparable between groups. The attenuated forearm vasoconstriction in young women was not observed in postmenopausal women (ΔBBFV -21 ± 5%). We concluded that young women have blunted forearm vasoconstriction in response to MVEEA compared with young men, and this effect is not evident in older postmenopausal women. These data suggest that female sex hormones dampen neurogenic vasoconstriction in response to apnea-induced hypoxemia.

Purpose: To compare ocular rigidity (OR) and outflow facility (C) coefficients in medically treated open-angle glaucoma (OAG) patients and controls, and to investigate differences in ocular pulse amplitude (OPA) and pulsatile ocular blood flow (POBF) between the two groups., Methods: Twenty-one OAG patients and 21 controls undergoing cataract surgery were enrolled. Patients with early or moderate primary or pseudoexfoliative OAG participated in the glaucoma group. A computer-controlled system, consisting of a pressure transducer and a microstepping device was employed intraoperatively. After cannulation of the anterior chamber, IOP was increased by infusing the eye with microvolumes of saline solution. IOP was recorded after each infusion step. At an IOP of 40 mm Hg, an IOP decay curve was recorded for 4 minutes. OR coefficients, C, OPA, and POBF were estimated from IOP and volume recordings., Results: There were no differences in age or axial length in the two groups. The OR coefficient was 0.0220 ± 0.0053 μl(-1) in the OAG and 0.0222 ± 0.0039 μl(-1) in the control group (P = 0.868). C was 0.092 ± 0.082 μL/min/mm Hg in the glaucoma group compared with 0.149 ± 0.085 μL/min/mm Hg in the control group at an IOP of 35 mm Hg (P < 0.001) and 0.178 ± 0.133 μL/min/mm Hg vs. 0.292 ± 0.166 μL/min/mm Hg, respectively, at an IOP of 25 mm Hg (P < 0.001). There were no differences in OPA or POBF between the two groups in baseline and increased levels of IOP (P > 0.05)., Conclusions: Manometric data reveal lower C in OAG patients and increased C with increasing IOP. There were no differences in the OR coefficient, OPA, and POBF between medically treated OAG patients and controls, failing to provide evidence of altered scleral distensibility and choroidal blood flow in OAG.

Hypertension is associated with reduced cerebral blood flow (CBF). Intensive (<130/80 mm Hg) blood pressure (BP) lowering in older people might give greater reduction in cardiovascular risk, but there are concerns that this might produce hypoperfusion which may precipitate falls and possibly stroke. We determined the effect of intensive compared with usual BP lowering on CBF in hypertensive older subjects. Individuals aged >70 years with a history of systolic hypertension on 1 or no BP lowering drugs were recruited from primary care (n=37; age, 75±4 years; systolic BP, >150 mm Hg) and randomized to receive intensive (target BP, <130/80 mm Hg) or usual (target BP, <140/85 mm Hg) BP lowering for 12 weeks, with reviews every 2 weeks. CBF, determined using 3T arterial spin labeling MRI, and 24-hour ambulatory BP were performed at baseline and after 12 weeks of treatment. Baseline BP (ambulatory or in clinic) and baseline gray matter CBF were not significantly different between the groups. After treatment, BP was reduced significantly in both groups but fell more in the intensive group (26/17 versus 15/5 mm Hg; P<0.01). Over the same period, gray matter CBF increased significantly in the intensive group (7±11 mL/min per 100 g; P=0.013) but was unchanged in the usual BP target group (-3±9 mL/min per 100 g; P=0.23); P<0.01 for comparison. Intensive BP lowering in older people with hypertension increases CBF, compared with BP lowering to usual target. These findings suggest hypertension in older people shifts the autoregulatory CBF curve rightward and downward and is reversible with BP lowering.

Key points We tested the hypothesis that in human hypertension, an increased tonicity/sensitivity of the peripheral chemoreflex causes a sympathetically mediated restraint of nutritive blood flow to the exercising muscles. Fourteen patients with treated hypertension (age 69 ± 11 years, 136 ± 12/80 ± 11 mmHg; mean ± SD) were studied under conditions of intravenous 0.9% saline (control) and low‐dose dopamine (2 µg kg−1 min−1) to inhibit the peripheral chemoreflex, at baseline, during isocapnic hypoxic rebreathing and during rhythmic handgrip exercise (3 min, 50% maximum voluntary contraction). At baseline, dopamine did not change mean blood pressure (95 ± 10 vs. 98 ± 10 mmHg, P = 0.155) but increased brachial artery blood flow (59 ± 20 vs. 48 ± 16 ml min−1, P = 0.030) and vascular conductance (0.565 ± 0.246 vs. 0.483 ± 0.160 ml min−1 mmHg−1; P = 0.039). Dopamine attenuated the increase in mean blood pressure (∆3 ± 4 vs. ∆8 ± 6 mmHg, P = 0.007) to isocapnic hypoxic rebreathing and reduced peripheral chemoreflex sensitivity by 28 ± 37% (P = 0.044). Rhythmic handgrip exercise induced increases in brachial artery blood flow and vascular conductance (both P < 0.05 vs. rest after 45 s) that were greater with dopamine than saline (e.g. Δ76 ± 54 vs. Δ60 ± 43 ml min−1 and Δ0.730 ± 0.440 vs. Δ0.570 ± 0.424 ml min−1 mmHg−1, respectively, at 60 s; main effect of condition both P < 0.0001). Our results indicate that the peripheral chemoreflex is tonically active at rest and restrains the blood flow and vascular conductance increases to exercise in treated human hypertension. It was hypothesised that in human hypertension, an increased tonicity/sensitivity of the peripheral chemoreflex causes a sympathetically mediated restraint of nutritive blood flow to the exercising muscles. Treated patients with hypertension (n = 14) were studied under conditions of intravenous 0.9% saline (control) and low‐dose dopamine (2 µg kg−1 min−1) to inhibit the peripheral chemoreflex. Low‐dose dopamine reduced resting ventilation and peripheral chemoreflex sensitivity, and while mean blood pressure was unchanged, brachial artery blood flow and vascular conductance were increased. Low‐dose dopamine augmented the brachial artery blood flow and vascular conductance responses to rhythmic handgrip. These findings indicate that the peripheral chemoreflex is tonically active at rest and restrains the blood flow, and vascular conductance increases to exercise in treated human hypertension. [ABSTRACT FROM AUTHOR]

The Windkessel (WK) model is a simplified mathematical model used to represent the systemic arterial circulation. While the WK model is useful for studying blood flow dynamics, it suffers from inaccuracies or uncertainties that should be considered when using it to make physiological predictions. This paper aims to develop an efficient and easy‐to‐implement uncertainty quantification method based on a local gradient‐based formulation to quantify the uncertainty of the pressure waveform resulting from aleatory uncertainties of the WK parameters and flow waveform. The proposed methodology, tested against Monte Carlo simulations, demonstrates good agreement in estimating blood pressure uncertainties due to uncertain Windkessel parameters, but less agreement considering uncertain blood‐flow waveforms. To illustrate our methodology's applicability, we assessed the aortic pressure uncertainty generated by Windkessel parameters‐sets from an available in silico database representing healthy adults. The results from the proposed formulation align qualitatively with those in the database and in vivo data. Furthermore, we investigated how changes in the uncertainty of the Windkessel parameters affect the uncertainty of systolic, diastolic, and pulse pressures. We found that peripheral resistance uncertainty produces the most significant change in the systolic and diastolic blood pressure uncertainties. On the other hand, compliance uncertainty considerably modifies the pulse pressure standard deviation. The presented expansion‐based method is a tool for efficiently propagating the Windkessel parameters' uncertainty to the pressure waveform. The Windkessel model's clinical use depends on the reliability of the pressure in the presence of input uncertainties, which can be efficiently investigated with the proposed methodology. For instance, in wearable technology that uses sensor data and the Windkessel model to estimate systolic and diastolic blood pressures, it is important to check the confidence level in these calculations to ensure that the pressures accurately reflect the patient's cardiovascular condition. [ABSTRACT FROM AUTHOR]

Optofluidic regulation of blood microflow in vivo represents a significant method for investigating illnesses linked to abnormal changes in blood circulation. Currently, non-invasive strategies are limited to regulation within capillaries of approximately 10 μm in diameter because the adaption to blood pressure levels in the order of several hundred pascals poses a significant challenge in larger microvessels. In this study, using laser-induced microbubble formation within microvessels of the mouse auricle, we regulate blood microflow in small vessels with diameters in the tens of micrometers. By controlling the laser power, we can control the growth and stability of microbubbles in vivo. This controlled approach enables the achievement of prolonged ischemia and subsequent reperfusion of blood flow, and it can also regulate the microbubbles to function as micro-pumps for reverse blood pumping. Furthermore, by controlling the microbubble, narrow microflow channels can be formed between the microbubbles and microvessels for assessing the apparent viscosity of leukocytes, which is 76.9 ± 11.8 Pa·s in the in vivo blood environment. The proposed design of in vivo microbubble valves opens new avenues for constructing real-time blood regulation and exploring cellular mechanics within living organisms. [ABSTRACT FROM AUTHOR]

The mechanism behind the acute reduction in peripheral arterial stiffness with reactive hyperemia is presumed to be flow-mediated; however, this has not been clearly demonstrated. We hypothesized that a larger reactive hyperemia magnitude would result in a greater reduction in peripheral arterial stiffness. Fourteen healthy young adults (5 females, 25 ± 5 yrs, mean ± SD) underwent reactive hyperemia with a rapid-release cuff on the upper arm inflated to 220 mmHg for 5 min: once with the arm positioned ~ 50ο above heart level and once with the arm positioned ~ 50ο below heart level. Brachial-radial pulse wave velocity (PWV) was measured with tonometers over brachial and radial arteries before cuff inflation and at 5, 15, and 30 min after release. Brachial blood flow was monitored with doppler ultrasound. At 5 min after reactive hyperemia, both the absolute (2.31 ± 1.22 vs 1.19 ± 1.19 m/sec, p = 0.007) and relative (24% vs 15%; p = 0.043) changes in brachial to radial PWV were greater with the arm below the heart compared to above the heart. The peak brachial blood flow was higher when the arm was below the heart compared to above the heart (477 ± 145 vs 369 ± 137 ml/min; p < 0.001). Reactive hyperemia acutely reduced peripheral arterial stiffness above and below heart level, with a greater decrease observed when the arm was positioned below the heart. These results demonstrate the contribution of conduit artery blood flow to the reduction of peripheral arterial stiffness after reactive hyperemia. [ABSTRACT FROM AUTHOR]

Introduction: Mechanical stresses and strains exerted on the glomerular cells have emerged as potentially influential factors in the progression of glomerular disease. Renal autoregulation, the feedback process by which the afferent arteriole changes in diameter in response to changes in blood pressure, is assumed to control glomerular mechanical stresses exerted on the glomerular capillaries. However, it is unclear how the two major mechanisms of renal autoregulation, the afferent arteriole myogenic mechanism and tubuloglomerular feedback (TGF), each contribute to the maintenance of glomerular mechanical homeostasis. Methods: In this study, we made a mathematical model of renal autoregulation and combined this model with an anatomically accurate model of glomerular blood flow and filtration, developed previously by us. We parameterized the renal autoregulation model based on data from previous literature, and we found evidence for an increased myogenic mechanism sensitivity when TGF is operant, as has been reported previously. We examined the mechanical effects of each autoregulatory mechanism (the myogenic, TGF and modified myogenic) by simulating blood flow through the glomerular capillary network with and without each mechanism operant. Results: Our model results indicate that the myogenic mechanism plays a central role in maintaining glomerular mechanical homeostasis, by providing the most protection to the glomerular capillaries. However, at higher perfusion pressures, the modulation of the myogenic mechanism sensitivity by TGF is crucial for the maintenance of glomerular mechanical homeostasis. Overall, a loss of renal autoregulation increases mechanical strain by up to twofold in the capillaries branching off the afferent arteriole. This further corroborates our previous simulation studies, that have identified glomerular capillaries nearest to the afferent arteriole as the most prone to mechanical injury in cases of disturbed glomerular hemodynamics. Discussion: Renal autoregulation is a complex process by whichmultiple feedback mechanisms interact to control blood flow and filtration in the glomerulus. Importantly, our study indicates that another function of renal autoregulation is control of themechanical stresses on the glomerular cells, which indicates that loss or inhibition of renal autoregulation may have a mechanical effect that may contribute to glomerular injury in diseases such as hypertension or diabetes. This study highlights the utility of mathematical models in integrating data from previous experimental studies, estimating variables that are difficult to measure experimentally (i.e. mechanical stresses in microvascular networks) and testing hypotheses that are historically difficult or impossible to measure. [ABSTRACT FROM AUTHOR]

This study was conducted to investigate the systemic hemodynamic and vascular changes in women during and after two commonly used clinical blood flow restriction (BFR) pressures at rest. There are minimal data regarding the independent effects of BFR on hemodynamic and systemic vascular changes due to pressor response, particularly among women. Therefore, this study investigated BFR‐induced alterations in pressor response and systemic flow redistribution at rest during two commonly used pressures (50% and 80% limb occlusion pressure [LOP]). Fifteen women (22.1 ± 4.2 years) completed two randomised sessions involving 8‐min of bilateral, lower limb restriction at 50% or 80% LOP followed by 8‐min of recovery post‐deflation. Changes in vascular (arterial diameter [DIA], time‐averaged mean velocity [TAMV], volume flow [VF], and area) and hemodynamic (heart rate [HR] and blood pressure) measures over time (pre‐, during, post‐occlusion) and by session (50% vs. 80% LOP) were tested using repeated measures analysis of variance. Repeated measures correlations (rrm) quantified common intraindividual associations between BFR‐induced hemodynamic and vascular responses. HR increased from baseline during 50% LOP and remained elevated during recovery (p < 0.05). HR increased from baseline during 80% LOP, while tibial VF and TAMV decreased (p < 0.03 for all). HR and TAMV values returned to baseline during recovery, while brachial artery VF decreased (p < 0.05). Changes in HR, brachial VF, and brachial TAMV were similar between 50% and 80% LOP (rrm = 0.32–0.70, p < 0.05 for all). At 80% LOP, changes in HR were positively correlated with brachial VF (rrm = 0.38) and TAMV (rrm = 0.43) and negatively correlated with tibial VF (rrm = −0.36) and TAMV (rrm = −0.30) (p < 0.05 for all). Results suggest that BFR at 80% LOP elicits an acute systemic pressor reflex without concomitant increases in brachial arterial flow, while 50% LOP elicits a subdued response. [ABSTRACT FROM AUTHOR]

Purpose: This study aimed to investigate differences in microvasculature dropout (MvD) between the superior and inferior hemispheres in glaucoma patients. Study design: Retrospective and cross-sectional. Methods: Fifty-eight eyes of 58 open-angle glaucoma patients (age 61.12 ± 10.19 years, mean deviation − 7.32 ± 6.36 dB) were included. MvD was detected with en face images from swept-source optical coherence tomography angiography. Blood flow at the optic nerve head was measured with laser speckle flowgraphy, represented as the mean blur rate in tissue (MBRT). Logistic and linear regression models adjusted for age, intraocular pressure, axial length, and circumpapillary retinal nerve fiber layer thickness were used to investigate the relationship between various factors and MvD angle in each hemisphere. Results: The presence of inferior MvD was related to peripapillary atrophy-β area (odds ratio = 14.10 [2.49–234.00], P = 0.019). Superior MvD angle was significantly related to MBRT in the superior quadrant (β = −0.31 [− 0.60 – −0.02], P = 0.037). Inferior MvD angle was significantly related to peripapillary atrophy-β area (β = 0.49 [0.21–0.77], P = 0.001). Conclusions: Only superior MvD demonstrated a significant relationship with reduced ocular blood flow. In contrast, inferior MvD was associated with mechanical stress. These findings may suggest a potential difference in pathophysiology between superior and inferior MvD. [ABSTRACT FROM AUTHOR]

Blood flow to the active muscles and arterial blood pressure (ABP) increase during dynamic exercise, whereas blood flow to inactive organs (e.g., splanchnic organs and inactive limbs) declines. Aging leads to exaggerated ABP responses to exercise in females, but whether this is related to greater splanchnic vasoconstriction is unknown. This study sought to clarify the effect of aging in females on celiac artery blood flow during dynamic light-intensity exercise. Twelve healthy young females (YF: 20 ± 2 yr, mean ± SD) and 12 healthy older females (OF: 71 ± 4 yr) performed dynamic knee-extension and knee-flexion exercises at 30% of heart rate reserve for 4 min. The absolute changes from baseline (Δ) for mean arterial blood pressure (MAP), celiac artery mean blood flow (celMBF), and celiac vascular conductance (celVC) during exercise were calculated. ABP was measured using an automated sphygmomanometer, and celMBF was recorded by Doppler ultrasonography. The increase in MAP during exercise was greater in OF than in YF (YF: +14 ± 7 mmHg, OF: +24 ± 13 mmHg, P = 0.028). The celMBF decreased during exercise in both groups, but there was no significant difference in the response between YF and OF (YF: −93.0 ± 66.1 mL/min, OF: −89.6 ± 64.0 mL/min, P = 0.951). The celVC also decreased during exercise and remained lower than baseline during exercise. However, the response was not different between YF and OF (YF: −1.8 ± 1.0 mL/min/mmHg, OF: −1.5 ± 0.6 mL/min/mmHg, P = 0.517). These results demonstrate that aging in females has minimal influence on splanchnic artery hemodynamic responses during dynamic light-intensity exercise, suggesting that exaggerated ABP responses during exercise in OF are not due to greater splanchnic vasoconstriction. NEW & NOTEWORTHY: During exercise, the splanchnic arteries vasoconstrict, contributing to blood flow redistribution and the blood pressure response. Blood pressure responses to exercise are exaggerated with aging in females; however, the physiological mechanism responsible has not been clarified. We show that celiac artery blood flow changes during light-intensity dynamic exercise do not differ with age in females. This indicates the exaggerated blood pressure to exercise with aging is likely not due to a difference in splanchnic vasoconstriction. [ABSTRACT FROM AUTHOR]

Systemic insulin increases muscle sympathetic nerve activity (MSNA) via both central actions within the brainstem and peripheral activation of the arterial baroreflex. Augmented MSNA during hyperinsulinemia likely restrains peripheral vasodilation and contributes to the maintenance of blood pressure (BP). However, in the absence of insulin action within the peripheral vasculature, whether central insulin stimulation increases MSNA and influences peripheral hemodynamics in humans remains unknown. Herein, we hypothesized intranasal insulin administration would increase MSNA and BP in healthy young adults. Participants were assigned to time control [TC, n = 13 (5 females/8 males), 28 ± 1 yr] or 160 IU of intranasal insulin administered over 5 min [n = 15 (5 females/10 males), 26 ± 2 yr]; five (1 female/4 males) participants completed both conditions. MSNA (fibular microneurography), BP (finger photoplethysmography), and leg blood flow (LBF, femoral Doppler ultrasound) were assessed at baseline, and 15 and 30 min following insulin administration. Leg vascular conductance [LVC = (LBF ÷ mean BP) × 100] was calculated. Venous insulin and glucose concentrations remained unchanged throughout (P > 0.05). Following intranasal insulin administration, MSNA (burst frequency; baseline = 100%; minute 15, 121 ± 8%; minute 30, 118 ± 6%; P = 0.009, n = 7) and mean BP (baseline = 100%; minute 15, 103 ± 1%; minute 30, 102 ± 1%; P = 0.003) increased, whereas LVC decreased (baseline = 100%; minute 15, 93 ± 3%; minute 30, 99 ± 3%; P = 0.03). In contrast, MSNA, mean BP, and LVC were unchanged in TC participants (P > 0.05). We provide the first evidence that intranasal insulin administration in healthy young adults acutely increases MSNA and BP and decreases LVC. These results enhance mechanistic understanding of the sympathetic and peripheral hemodynamic response to insulin. NEW & NOTEWORTHY: Systemic insulin increases muscle sympathetic nerve activity (MSNA) via central actions within the brainstem and peripheral activation of the arterial baroreflex. In the absence of peripheral insulin action, whether central insulin stimulation increases MSNA and influences peripheral hemodynamics in humans was unknown. We provide the first evidence that intranasal insulin administration increases MSNA and blood pressure and reduces leg vascular conductance. These results enhance mechanistic understanding of the sympathetic and hemodynamic response to insulin. [ABSTRACT FROM AUTHOR]

Abstract The mechanism behind the acute reduction in peripheral arterial stiffness with reactive hyperemia is presumed to be flow-mediated; however, this has not been clearly demonstrated. We hypothesized that a larger reactive hyperemia magnitude would result in a greater reduction in peripheral arterial stiffness. Fourteen healthy young adults (5 females, 25 ± 5 yrs, mean ± SD) underwent reactive hyperemia with a rapid-release cuff on the upper arm inflated to 220 mmHg for 5 min: once with the arm positioned ~ 50ο above heart level and once with the arm positioned ~ 50ο below heart level. Brachial-radial pulse wave velocity (PWV) was measured with tonometers over brachial and radial arteries before cuff inflation and at 5, 15, and 30 min after release. Brachial blood flow was monitored with doppler ultrasound. At 5 min after reactive hyperemia, both the absolute (2.31 ± 1.22 vs 1.19 ± 1.19 m/sec, p = 0.007) and relative (24% vs 15%; p = 0.043) changes in brachial to radial PWV were greater with the arm below the heart compared to above the heart. The peak brachial blood flow was higher when the arm was below the heart compared to above the heart (477 $$\pm$$ ± 145 vs 369 $$\pm$$ ± 137 ml/min; p

Cervical spinal cord injury usually results in cardiorespiratory dysfunctions due to interruptions of the bulbospinal pathways innervating the cervical phrenic motoneurons and thoracic sympathetic preganglionic neurons. The present study aimed to evaluate the therapeutic effects of adrenergic agents on systemic and spinal hemodynamics during acute cervical spinal cord injury. In vivo animal study. The cardiorespiratory function and spinal cord blood flow and oxygenation level were monitored in response to cervical spinal cord contusion and intravenous infusion of three types of adrenergic agents (phenylephrine, dobutamine, and norepinephrine). Cervical spinal cord contusion resulted in immediate reduction of respiratory airflow, arterial blood pressure, and spinal cord blood flow. The arterial blood pressure and spinal cord blood flow remained lower than the preinjury value in contused animals infused with saline at 60 min postinjury. Infusion of phenylephrine (500, 1000, and 2000 μg/kg) and norepinephrine (125, 250, and 500 μg/kg) significantly increased the arterial blood pressure, while only norepinephrine augmented the spinal cord blood flow. Conversely, dobutamine (1000 and 2000 μg/kg) reduced both arterial blood pressure and spinal cord blood flow. Notably, administration of adrenergic agents tended to increase spinal cord hemorrhage in contused animals. Infusion of norepinephrine can effectively maintain the blood pressure and improve spinal cord blood flow during acute spinal cord injury. Norepinephrine may be a superior medicine for hemodynamic management; however, the potential hemorrhage should be considered when utilizing the vasopressor to regulate systemic and spinal hemodynamics at the acute injured stage. [ABSTRACT FROM AUTHOR]

Background/Aims: The growing prevalence of sedentary behaviour across the life course is linked to an increased risk of chronic venous disease and related mortality, warranting the need for non-invasive interventions to improve blood flow and lower extremity function. The aim of this study was to investigate the change in venous blood flow, heart rate and blood pressure after 8 minutes of using the Leeper device, Circulation Booster and light intensity walking. Methods: A quasi-experimental crossover study involving 11 participants (eight women, three men, mean age 23.91 years, standard deviation 1.04 years) was conducted using Leeper and Circulation Booster devices and light intensity walking. During each intervention, participants exercised for 8 minutes, and blood flow was recorded at 0, 4 and 8 minutes. Heart rate and blood pressure were recorded at 0 and 8 minutes. Blood flow was the primary outcome measure, and heart rate and blood pressure were secondary outcomes. Participants rested for 10 minutes between exercise. A two-way repeated measures analysis of variance was used to analyse the effect of intervention and time on blood flow, blood pressure and heart rate. Results: There was no significant interaction between intervention and time on blood flow (P=0.180) indicating that blood flow did not change over time depending on intervention. There was no significant main effect of time on blood flow (P=0.206), indicating that no intervention caused a significant increase or decrease in blood flow after 8 minutes of exercise. Conclusions: The interventions involving the Leeper and Circulation Booster devices and light intensity walking did not appear to significantly increase blood flow in young adults. Further studies involving participants from older age groups and those with pathological interventions are warranted to examine the potential effectiveness of these interventions. Implications for practice: The findings may assist with the advice that allied health professionals provide regarding the use of seated exercise trainers and EMS devices and their ability to influence changes in blood flow. [ABSTRACT FROM AUTHOR]

To compare blood pressure (BP), intraocular pressure (IOP), ophthalmic artery flow (OAF) velocity, retinal nerve fiber layer (RNFL) thickness, and visual fields in newly diagnosed hypertension (HT) patients (before treatment), chronic HT (on antihypertensive medications >5 years) and normotensives. A prospective, cross-sectional study at a tertiary care centre in India. Three groups of 45 patients each: group 1 - early HT, group 2 - chronic HT, and Group 3 - normotensives, underwent evaluation of BP, IOP by Goldmann applanation tonometry (GAT), OAF velocity by transcranial doppler (TCD), RNFL analysis by spectral-domain optical coherence tomography (SD-OCT), and visual fields. The BP was highest in early HT > chronic HT > normotensives (p < 0.001). The IOP of early HT, chronic HT, and normotensives were 15.87 ± 2.19 mmHg, 13.47 ± 1.92 mmHg, and 15.67 ± SD 1.75 mmHg (p < 0.001). The OAF velocity [peak systolic velocity (PSV), end-diastolic velocity (EDV) in cm/sec] was lowest in chronic HT (30.80 ± 7.05, 8.58 ± 1.58) < early HT (35.47 ± 5.34, 10.02 ± 1.74) < normotensives (36.29 ± 4.43, 10.44 ± 2.29), (p < 0.001). The average RNFL thickness was significantly lower in chronic HT (p = 0.022). The PSV, EDV, and MFV showed significant correlation with IOP (r = 0.247, p = 0.004; r = 0.206, p = 0.016; r = 0.266, p = 0.002) and average RNFL thickness (r = 0.309, p= <0.001; r = 0.277, p = 0.001; r = 0.341, p < 0.001) Patients with chronic HT demonstrated the lowest retrobulbar flows, IOP and lower RNFL measurements. Lower ocular perfusion may be associated with lower IOP and may be a risk factor for end-organ damage (RNFL) independent of IOP. [ABSTRACT FROM AUTHOR]

Introduction: Blood Flow Restriction Training (BFRT) was developed by Southeast Asia Treaty Organisation (SATO) in Japan in 1966. BFRT is a method that mimics the effects of high-intensity training by combining low-intensity exercise with blood flow obstruction. It involves limb compression using compression cuffs to limit venous outflow and minimise arterial inflow during rehabilitation training. By allowing individuals to lift smaller loads and increase strength training gains, BFRT can reduce the overall stress exerted on the limb. Aim: To assess the difference in muscle girth and blood pressure after a single bout of BFRT. Materials and Methods: This was a single-blinded, singlesite pretest, post-test quasi-experimental study. A total of 30 subjects were enrolled (16 females and 14 males) between the ages of 18 to 25 years. This study was conducted at the Department of Physiotherapy, Galgotias University, Greater Noida, Uttar Pradesh, India. Outcome measures included muscle girth measured using a flexible tape and blood pressure using an automatic oscillometric device (Omron Hem 7113, São Paulo, Brazil). Paired t-test and Wilcoxon test were performed using Statistical Package for Social Sciences (SPSS) software version 20.0. Results: It was found that an acute bout of BFRT caused improvement in all outcome measures. There was a statistically significant increase in muscle girth and blood pressure after BFRT (p-value<0.001). Conclusion: There was a significant increase in blood pressure (both Systolic Blood Pressure (SBP) and Diastolic Blood Pressure (DBP)) and muscle girth after BFRT with no reported adverse effects. [ABSTRACT FROM AUTHOR]

Background: Arterial blood pressure (ABP) is essential to provide adequate perfusion pressure and blood flow to tissues. Usually, ABP is tightly controlled through a variety of complex physiological mechanisms, and significant deviation of ABP from normal may result in end‐organ damage. Measurement of ABP is relatively straightforward and can be used to assess cardiovascular function and guide therapeutic decisions. Challenges in the interpretation of ABP may arise due to individual patient factors and may be dependent on the method of measurement. Aim of the article: This article is the first in a two‐part series and aims to review the physiology and measurement of arterial blood pressure in small animal practice. The second article, to be published in a subsequent issue of In Practice, will focus on the pathophysiology of hypotension and the options for treatment. [ABSTRACT FROM AUTHOR]

Background: In bypass surgery for moyamoya disease (MMD), the superficial temporal artery's (STA) pressure needs to surpass that of the cortical M4 recipient of the middle cerebral artery (MCA), boosting cerebral blood flow into the MCA and enhancing cerebral circulation. This study investigates the STA-MCA arterial pressure parameters and gradients during bypass surgery, aiming to deepen our understanding of hemodynamic shifts pre- and post-operation. Methods: DSA imaging data were prospectively collected from patients diagnosed with bilateral MMD who underwent STA-MCA bypass surgery between 2022 and 2023 and stratified according to the Suzuki stage. The mean arterial pressure (MAP) of the donor and recipient arteries was directly measured during the STA-MCA bypass procedure, and these data were statistically analyzed and evaluated. Results: Among 48 MMD patients, Suzuki grading revealed that 43.8% were in early stages (II and III), while 56.2% were in advanced stages (IV, V, and VI). Predominantly, 77.1% presented with ischemic-type MMD and 22.9% with hemorrhagic type. Pre-bypass assessments showed that 62.5% exhibited antegrade blood flow direction, and 37.5% had retrograde. The mean recipient artery pressure was 35.0 ± 2.3 mmHg, with a mean donor-recipient pressure gradient (δP) of 46.4 ± 2.5 mmHg between donor and recipient arteries. Post-bypass, mean recipient artery pressure increased to 73.3 ± 1.6 mmHg. No significant correlation (r = 0.18, P = 0.21) was noted between δP and Suzuki staging. Conclusion: Our study elucidated that cerebral blood pressure significantly decreases beyond the moyamoya network at the distal M4 segment. Furthermore, we observed bidirectional flow in MCA territories and a significant positive pressure gradient between the STA and M4 segments. The lack of correlation between Suzuki stages and M4 pressures indicates that angiographic severity may not reflect hemodynamic conditions before surgery, highlighting the need for customized surgical approaches. [ABSTRACT FROM AUTHOR]

Purpose: Self-myofascial release (SMR) is a form of self-massage aiming to release tension, improve blood flow, and alleviate muscle soreness. This study aimed to determine whether a single session of SMR could impact cardiovascular parameters at rest and during a cold pressor test (CPT). Methods: Twenty male participants (aged 26 ± 2 years) underwent a 20-min SMR and a 20-min seated control condition (CON) on two separate test days in a randomized order. Peripheral and central blood pressure (BP), total peripheral resistance (TPR), pulse wave velocity (PWV), heart rate (HR), root mean square of successive RR interval differences (RMSSD), and the quotient of low-frequency power and high-frequency power (LF/HF) were measured both at rest and during a CPT before (t0), 2 min (t1), and 20 min (t2) after the SMR and CON. Results: Time × condition interactions could be detected for peripheral and central diastolic BP, TPR, HR, and RMSSD. Following the SMR, peripheral diastolic BP, central diastolic BP, TPR, and RMSSD were reduced, while HR was increased compared to the CON. Regarding the CPT time × condition interactions could be detected for peripheral, and central diastolic BP, with lower values after SMR. Conclusion: The results of the present study suggest that a single bout of SMR confers favorable cardiovascular benefits in healthy normotensive individuals. Furthermore, SMR can attenuate the hemodynamic reactivity to a stress test. Future research should address whether regular SMR leads to chronic adaptations similar to regular, moderate aerobic exercise, massage therapy, and static stretching. [ABSTRACT FROM AUTHOR]

Continuous non-invasive blood pressure (CNBP) monitoring is of the utmost importance in detecting and managing hypertension, a leading cause of death in the United States. Extensive research has delved into pioneering methods for predicting systolic and diastolic blood pressure values by leveraging pulse arrival time (PAT), the time difference between the proximal and distal signal peaks. The most widely employed pairing involves electrocardiography (ECG) and photoplethysmography (PPG). Possessing similar characteristics in terms of measuring blood flow changes, a recently investigated optical signal known as speckleplethysmography (SPG) showed its stability and high signal-to-noise ratio compared with PPG. Thus, SPG is a potential surrogate to pair with ECG for CNBP estimation. The present study aims to unlock the untapped potential of SPG as a signal for non-invasive blood pressure monitoring based on PAT. To ascertain SPG's capabilities, eight subjects were enrolled in multiple recording sessions. A third-party device was employed for ECG and PPG measurements, while a commercial device served as the reference for arterial blood pressure (ABP). SPG measurements were obtained using a prototype smartphone-based system. Following the completion of three scenarios—sitting, walking, and running—the subjects' signals and ABP were recorded to investigate the predictive capacity of systolic blood pressure. The collected data were processed and prepared for machine learning models, including support vector regression and decision tree regression. The models' effectiveness was evaluated using root-mean-square error and mean absolute percentage error. In most instances, predictions utilizing P A T S P G exhibited comparable or superior performance to P A T P P G (i.e., SPG Rest ± 12.4 mmHg vs. PPG Rest ± 13.7 mmHg for RSME, and SPG 8% vs. PPG 9% for MAPE). Furthermore, incorporating an additional feature, namely the previous SBP value, resulted in reduced prediction errors for both signals in multiple model configurations (i.e., SPG Rest ± 12.4 mmHg to ±3.7 mmHg for RSME, and SPG Rest 8% to 3% for MAPE). These preliminary tests of SPG underscore the remarkable potential of this novel signal in PAT-based blood pressure predictions. Subsequent studies involving a larger cohort of test subjects and advancements in the SPG acquisition system hold promise for further improving the effectiveness of this newly explored signal in blood pressure monitoring. [ABSTRACT FROM AUTHOR]

Purpose: Autonomic control of orofacial areas is an integral part of the stress response, controlling functions such as pupil dilatation, salivation, and skin blood flow. However, the specific control of blood flow in head muscles during stress is unknown. This study aims to investigate the hemodynamic response of temporalis and masseter muscles in response to five different stressors. Methods: Sixteen healthy individuals were subjected to a randomized series of stressors, including cold pressor test, mental arithmetic test, apnea, isometric handgrip, and post-handgrip muscle ischemia, while in the sitting posture. Finger-pulse photoplethysmography was used to measure arterial blood pressure, heart rate, and cardiac output. Near-infrared spectroscopy was used to measure changes in tissue oxygenation and hemoglobin indices from the temporalis and masseter muscles. Results: All stressors effectively and significantly increased arterial blood pressure. Tissue oxygenation index significantly increased in both investigated head muscles during mental arithmetic test (temporalis: 4.22 ± 3.52%; masseter: 3.43 ± 3.63%) and isometric handgrip (temporalis: 3.45 ± 3.09%; masseter: 3.26 ± 3.07%), suggesting increased muscle blood flow. Neither the masseter nor the temporalis muscles evidenced a vasoconstrictive response to any of the stressors tested. Conclusion: In the different conditions, temporalis and masseter muscles exhibited similar hemodynamic patterns of response, which do not include the marked vasoconstriction generally observed in limb muscles. The peculiar sympathetic control of head muscles is possibly related to the involvement of these muscles in aggressive/defensive reactions and/or to their unfavorable position with regard to hydrostatic blood levels. [ABSTRACT FROM AUTHOR]

Purpose: This research aims to study and compare the effects of moderateintensity continuous exercise and accumulated exercise with different number of bouts on common carotid arterial stiffness and hemodynamic variables. Methods: Thirty healthy male adults were recruited to complete four trials in a randomized crossover design: no-exercise (CON); continuous exercise (CE, 30-min cycling); accumulated exercise including two or three bouts with 10-min rest intervals (AE15, 2 × 15-min cycling; AE10, 3 × 10-min cycling). The intensity in all the exercise trials was set at 45%-55% heart rate reserve. Blood pressure, right common carotid artery center-line velocity, and arterial inner diameter waveforms were measured at baseline and immediately after exercise (0 min), 10 min, and 20 min. Results: 1) The arterial stiffness index and pressure-strain elastic modulus of the CE and AE15 groups increased significantly at 0 min, arterial diameters decreased in AE15 and AE10, and all indicators recovered at 10 min. 2) The mean blood flow rate and carotid artery center-line velocity increased in all trials at 0 min, and only the mean blood flow rate of AE10 did not recover at 10 min. 3) At 0 min, the blood pressure in all trials was found to be increased, and the wall shear stress and oscillatory shear index of AE10 were different from those in CE and AE15. At 20 min, the blood pressure of AE10 significantly decreased, and the dynamic resistance, pulsatility index, and peripheral resistance of CE partially recovered. Conclusion: There is no significant difference in the acute effects of continuous exercise and accumulated exercise on the arterial stiffness and diameter of the carotid artery. Compared with continuous exercise, accumulated exercise with an increased number of bouts is more effective in increasing cerebral blood supply and blood pressure regulation, and its oscillatory shear index recovers faster. However, the improvement of blood flow resistance in continuous exercise was better than that in accumulated exercise. [ABSTRACT FROM AUTHOR]

Vascular dysfunction contributes to the development of osteopenia in hypertensive patients, as decreased blood supply to bones results in tissue damage and dysfunction. The effect of anti-hypertensive medicines on bone mass in hypertensive individuals is inconclusive because of the varied mechanism of their action, and suggests that reducing blood pressure (BP) alone is insufficient to enhance bone mass in hypertension. Pentoxifylline (PTX), a hemorheological drug, improves blood flow by reducing blood viscosity and angiogenesis, also has an osteogenic effect. We hypothesized that improving vascular function is critical to increasing bone mass in hypertension. To test this, we screened various anti-hypertensive drugs for their in vitro osteogenic effect, from which timolol and hydralazine were selected. In adult female spontaneously hypertensive rats (SHRs), timolol and hydralazine did not improve vascular function and bone mass, but PTX improved both. In female SHR animals, PTX restored bone mass, strength and mineralization, up to the level of normotensive control rats. In addition, we observed lower blood vasculature in the femur of adult SHR animals, and PTX restored them. PTX also restored the bone vascular and angiogenesis parameters that had been impaired in OVX SHR compared to sham SHR. This study demonstrates the importance of vascular function in addition to increased bone mass for improving bone health as achieved by PTX without affecting BP, and suggests a promising treatment option for osteoporosis in hypertensive patients, particularly at-risk postmenopausal women. [ABSTRACT FROM AUTHOR]

Purpose: Taking a short rest after lunch suppresses increases in blood flow to the digestive organs and maintains blood flow to the brain in the afternoon, possibly providing beneficial effects in preventing post-prandial drowsiness. The present study investigated sex-dependent influences on changes in hemodynamics produced by taking a short rest after lunch. Methods: Subjects comprised 20 healthy young adults (10 men, 10 women; mean age 21 ± 1 years). Doppler sonography was performed to measure blood flow in the superior mesenteric artery (SMA) and common carotid artery (CCA) before and after lunch every hour on each day, with and without a 15-min rest with eyes closed after lunch. Blood pressure and heart rate (HR) were also measured. Results: For both men and women, peak systolic velocity (PSV) in the SMA was suppressed by taking a rest. PSV in the CCA in men was increased at 0.5 h after lunch in the resting condition but was decreased in the non-resting condition (median 109%, interquartile range [IQR] 102–120% vs. median 98%, IQR 90–107%; P = 0.037). No such differences were observed in women. Although post-prandial increases in HR were observed in women, a similar increase was only found for men in the resting condition. Conclusion: An increase in CCA blood flow was observed only in men. The present study suggests that a short rest after lunch could better promote the maintenance of blood flow to the brain in men than in women. [ABSTRACT FROM AUTHOR]

Acute proximal superior mesenteric artery (SMA) occlusion is highly lethal, and adjuncts are needed to mitigate ischemic injury until definitive therapy. We hypothesized that raising mean arterial pressure (MAP) >90 mmHg with norepinephrine may delay irreversible bowel ischemia by increasing gastroduodenal artery (GDA) flow despite possible pressor-induced vasospasm. 12 anesthetized swine underwent laparotomy, GDA flow probe placement, and proximal SMA exposure and clamping. Animals were randomized between conventional therapy (CT) versus targeted MAP >90 mmHg (MAP push; MP) where norepinephrine was titrated after 45 min of SMA occlusion. Animals were followed until bowel death or 4 h. Kaplan–Meier bowel survival, mean normalized GDA flow, and histology were compared. 12 swine (mean 57.8 ± 7.6 kgs) were included, six per group. Baseline weight, HR, MAP and GDA flows were not different. Within 5 min following SMA clamping, all 12 animals had an increase in MAP without other intervention from 81.7 to 105.5 mmHg (29.1%, P < 0.01) with a concomitant 74.9% increase in GDA flow as compared to baseline (P < 0.01). Beyond 45 min postclamp, MAP was greater in the MP group as intended, as were GDA flows. Median time to irreversibly ischemic bowel was 31% longer for MAP push animals (CT: 178 versus MP: 233 min, P = 0.006), Hazard Ratio of CT 8.85 (95% CI: 1.86-42.06); 3/6 MP animals versus 0/6 CT animals with bowel survived to predetermined end point. In this swine model of acute complete proximal SMA occlusion, increasing MAP >90 mmHg with norepinephrine was associated with an increase in macrovascular blood flow through the GDA and bowel survival. Norepinephrine was not associated with worse bowel survival and a MAP push may increase the time window where ischemic bowel can be salvaged. [ABSTRACT FROM AUTHOR]