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This study aimed to assess the relationship between the foetal superior mesenteric artery (SMA) Doppler and the time to first meconium passage (FMP) in foetuses with late-onset foetal growth restriction. This single-centre, prospective, observational, cohort study included 57 patients with late-onset FGR. The newborn infants were divided into two groups: preterm (36.8%) and term (63.2%). The time to FMP of the infants was compared to the foetal SMA parameters obtained within a week before delivery. The median time to FMP was similar between two groups ( p  = .31). The SMA pulsatility index (PI) was higher in the preterm group ( p  < .01). There was no correlation between foetal SMA PI or resistance index and time to FMP. In late-onset FGR infants, our study found no association between SMA Doppler measurements and time to FMP. However, a significant difference was detected in SMA PI between preterm and term infants. Impact Statement What is already known in this subject? Foetal growth restriction (FGR) can affect splanchnic circulation of the foetus and this alteration can be associated with some disorders including necrotising enterocolitis. What do the results of this study add? Superior mesenteric artery (SMA) Doppler indices are not associated with first meconium passage in neonates with late-onset foetal growth restriction. The pulsatility index of SMA is significantly higher in foetuses delivered before term. What are the implications of these findings for clinical practice and/or further research? Further research should be conducted to investigate the relationship between foetal SMA Doppler indices and neonatal gastrointestinal morbidities in foetuses with early onset FGR with Doppler anomalies. These studies can shed light from the prenatal to the postnatal period, allowing clinicians to predict potential problems and take precautions.

Objectives: Medieval yoga texts claim that a special exercise of the muscles of the anterior abdominal wall, called agnisara, improves digestive function. Main objective of the study was to demonstrate change in the blood flow through superior mesenteric artery (if any) after performance of agnisara., Methods: Ultrasound examination of the linear and volumetric indicators of blood flow in the superior mesenteric artery (SMA) before and after performing the agnisara yoga exercise 100 times was carried out in 12 healthy volunteers of both sexes (8 of them women)., Results: A significant increase in the diameter of the SMA, peak systolic and diastolic velocities, and blood flow in the superior mesenteric artery after performing the agnisara exercise 100 times was found, which contrasts with the established data on a decrease in splanchnic blood flow in humans in response to normal physical activity., Conclusion: Properly performed agnisara increases blood flow to the splanchnic region, registered by the SMA, which should contribute to adequate blood supply to the gastrointestinal tract for successful performance of digestive function., Competing Interests: Declaration of competing interest None declared., (Copyright © 2022. Published by Elsevier Ltd.)

Acrolein, an electrophilic α,β-unsaturated aldehyde, is present in foods and beverages, and is a product of incomplete combustion, and thus, reaches high ppm levels in tobacco smoke and structural fires. Exposure to acrolein is linked with cardiopulmonary toxicity and cardiovascular disease risk. The hypothesis of this study is the direct effects of acrolein in isolated murine blood vessels (aorta and superior mesenteric artery, SMA) are transient receptor potential ankyrin-1 (TRPA1) dependent. Using isometric myography, isolated aorta and SMA were exposed to increasing levels of acrolein. Acrolein inhibited phenylephrine (PE)-induced contractions (approximately 90%) in aorta and SMA of male and female mice in a concentration-dependent (0.01-100 μM) manner. The major metabolite of acrolein, 3-hydroxypropylmercapturic acid (3HPMA), also relaxed PE-precontracted SMA. As the SMA was 20× more sensitive to acrolein than aorta (SMA EC 50 0.8 ± 0.2 μM; aorta EC 50  > 29.4 ± 4.4 μM), the mechanisms of acrolein-induced relaxation were studied in SMA. The potency of acrolein-induced relaxation was inhibited significantly by: 1) mechanically-impaired endothelium; 2) Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME); 3) guanylyl cyclase (GC) inhibitor (ODQ); and, 4) a TRPA1 antagonist (A967079). TRPA1 positive immunofluorescence was present in the endothelium. Compared with other known TRPA1 agonists, including allyl isothiocyanate (AITC), cinnamaldehyde, crotonaldehyde, and formaldehyde, acrolein stimulated a more potent TRPA1-dependent relaxation. Acrolein, at high concentration [100 μM], induced tension oscillations (spasms) independent of TRPA1 in precontracted SMA but not in aorta. In conclusion, acrolein is vasorelaxant at low levels (physiological) yet vasotoxic at high levels (toxicological)., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Purpose: Monitoring disease progression is crucial to improve the outcome of necrotizing enterocolitis (NEC). A previous study indicates that intestinal wall flow velocity was reduced in NEC pups from the initial stages of the disease. This study aims to investigate whether splanchnic perfusion via the superior mesenteric artery (SMA) (i) is altered during NEC development and (ii) can be used as a monitoring tool to assess disease progression., Methods: NEC was induced in C57BL/6 mice via gavage feeding of formula, hypoxia, and oral lipopolysaccharide, from postnatal day 5 (P5) to P9 (AUP: 32,238). Breastfed littermates served as controls. Doppler ultrasound (U/S) of bowel loops was performed daily. Intestinal wall perfusion was calculated as average flow velocity (mm/s) of multiple abdominal regions. Groups were compared using one-way ANOVA., Results: The SMA flow velocity was not altered during the initial stage of NEC development, but become significantly reduced at P8 when the intestinal disease was more advanced. These changes occurred concomitantly with an increase in heart rate., Conclusions: NEC is associated with intestinal hypo-perfusion at the periphery and flow in the SMA is reduced during the later stages of disease indicating the presence of intestinal epithelium damage. This study contributes to understanding NEC pathophysiology and illustrates the value of Doppler U/S in monitoring disease progression.

The vascular action of trimethylamine-N-oxide (TMAO)-the gut microbiota-derived metabolite-in contributing cardiovascular disease is a controversial topic. A recent study has shown that acute exposure of TMAO at moderate concentrations inhibits endothelium-dependent hyperpolarization (EDH)-type relaxations selectively in rat isolated femoral arteries, but not in mesenteric arteries. Here we determined the efficacy of higher TMAO concentrations with longer exposure times on vascular reactivity in rat isolated superior mesenteric arteries. Acetylcholine-induced EDH-type relaxations were examined before and after incubation with TMAO (0.1-10 mM) at increasing exposure times (1-24 h). One- and 4-h-incubations with TMAO at 0.1-3 mM did not cause any change in EDH-type relaxations. However, when the incubation time was increased to 24 h, responses to acetylcholine were reduced in arteries incubated with 1-3 mM TMAO. In addition, at higher TMAO concentration (10 mM) the decrease in EDH relaxations could be detected both in 4-h- and 24-h-incubations. The EDH-relaxations were preserved in rings incubated with 10 mM TMAO for 24 h in the presence of SKA-31 (10 µM), the small (SKCa)- and intermediate (IKCa)-conductance calcium-activated potassium channel activator. Contractile responses to phenylephrine increased in arteries exposed to 10 mM TMAO for 24 h. Interestingly, nitric oxide (NO)-mediated relaxations remained unchanged in arteries treated for 24 h at any TMAO concentration. Our study revealed that TMAO selectively disrupted EDH-type relaxations time-dependently without interfering with NO-induced vasodilation in rat isolated mesenteric arteries. Disruption of these relaxations may help explain the causal role of elevated TMAO levels in certain vascular diseases.

Context: Exposure of the small intestine to nutrients frequently leads to marked reductions in blood pressure (BP) in type 2 diabetes (T2DM). It remains unclear whether the region of the gut exposed to nutrients influences postprandial cardiovascular responses., Objective: To evaluate the cardiovascular responses to proximal and distal small intestinal glucose infusion in health and T2DM., Design: Double-blind, randomized, crossover design., Setting: Single center in Australia., Patients: 10 healthy subjects and 10 T2DM patients., Interventions: Volunteers were studied on 2 occasions, when a transnasal catheter was positioned with infusion ports opening 13 cm and 190 cm beyond the pylorus. A 30-g bolus of glucose was infused into either site and 0.9% saline into the alternate site over 60 minutes., Main Outcome Measures: BP, heart rate (HR), and superior mesenteric artery (SMA) blood flow were measured over 180 minutes., Results: Systolic BP was unchanged in response to both infusions in health, but decreased in T2DM, with a greater reduction after proximal versus distal infusion (all P ≤ .01). The increment in HR did not differ between treatments in health, but was greater after distal versus proximal infusion in T2DM (P = .02). The increases in SMA blood flow were initially greater, but less sustained, with proximal versus distal infusion in health (P < .001), a pattern less evident in T2DM., Conclusions: In T2DM, postprandial hypotension may be mitigated by diversion of nutrients from the proximal to the distal small intestine., (© Endocrine Society 2020. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Aims: β-Adrenoceptors (β-ADRs) mediating the relaxation of rat superior mesenteric arteries (SMAs) were pharmacologically identified, and the effects of chemical sympathetic denervation on β-ADR-mediated relaxation were examined., Main Methods: The tension changes of endothelium-denuded SMAs were isometrically recorded and the mRNA of endothelium-denuded SMA β-ADR was detected using RT-PCR., Key Findings: In endothelium-denuded SMAs contracted with ≥10 -7  M phenylephrine (an α 1 -ADR agonist), isoprenaline (a β-ADR agonist)-induced relaxation was competitively inhibited by 3 × 10 -9 -10 -8  M propranolol (a β 1,2 -ADR antagonist), but not further affected by ≥10 -8  M propranolol. Although isoprenaline-induced relaxation was not affected by ICI-118,551 (10 -9 -10 -8  M; a β 2 -ADR antagonist), it was competitively inhibited by atenolol (10 -7 -3 × 10 -7  M; a β 1 -ADR antagonist) in the presence of ICI-118,551. In the presence of 10 -7  M propranolol, isoprenaline- and CGP-12177A (a β 3 -ADR partial agonist)-induced relaxation was competitively inhibited by high concentrations of bupranolol (a β 1,2,3 -ADR antagonist), with pA 2 values of 6.49 and 5.76, respectively. We detected the mRNA of β 1 - and β 3 -ADRs in endothelium-denuded SMAs. Treatment with 6-hydroxydopamine (a catecholaminergic neurotoxin) reduced maximal isoprenaline-induced relaxation in the presence and absence of 10 -7  M propranolol, but not CGP-12177A-induced relaxation., Significance: Isoprenaline-induced relaxation of rat SMAs is mediated by β 1 - and β 3 -ADRs. β-ADR-mediated relaxation of rat SMAs is shown to be attenuated by chemical sympathetic denervation. The differences in the effects of bupranolol and chemical sympathetic denervation on the responses to isoprenaline and CGP-12177A in rat SMAs might be explained by the possible presence of multiple β 3 -ADRs with different pharmacological properties., (Copyright © 2019. Published by Elsevier Inc.)

Background: An accessory middle colic artery (AMCA) is an aberrant artery feeding the splenic flexure of the colon. Little is known about the branching pattern of an AMCA. We aimed to evaluate the branching pattern of the AMCA from the superior mesenteric artery (SMA) with special reference to the pancreatic artery using multidetector-row computed tomography (MDCT) before surgery., Methods: We investigated 112 patients who underwent contrast-enhancement MDCT before surgical resection of the pancreas between January 2015 and July 2018. The pancreatic branch from the AMCA was divided into the dorsal pancreatic artery (DPA) and the inferior pancreaticoduodenal artery (IPDA). The branching level and angle of the AMCA from the SMA were also evaluated., Results: The AMCA was present in 27.7% of patients (n = 31/112). The AMCA branching pattern was classified into four types: type A, no branch from the AMCA (n = 20); type B, a common trunk with the DPA (n = 6); type C, a common trunk with the IPDA (n = 3); and type D, a common trunk with the DPA and IPDA (n = 2). The AMCA with the IPDA (types C and D) branched more proximally compared to the AMCA without the IPDA (P = 0.04). The AMCA branched vertically from the SMA in most cases (n = 24/31, 77.4%)., Conclusions: The AMCA had a pancreatic branch in 8.9% (10/112) of cases. Special attention should be paid to its branching pattern in pancreatic and colon surgery., (Copyright © 2019 IAP and EPC. Published by Elsevier B.V. All rights reserved.)

Hemodynamics is subject to change after eating meals, which may be related to various postprandial physical statuses such as hypotension or daytime sleepiness. Previous studies have shown that blood flow in the superior mesenteric artery (SMA) increases after meals, but conflicting results have been reported regarding blood flow in the common carotid artery (CCA). In those studies, the fasting interval before the meal was not taken into account. For example, eating breakfast shortly before lunch may affect hemodynamics in these vessels. The present study therefore investigated hemodynamics in the CCA and SMA after lunch, comparing cases with and without breakfast. Subjects comprised 24 healthy young adults (mean age, 22 ± 1 years). Duplex Doppler sonography was performed to measure blood flow values for calculating flow volume (FV) before and after lunch until 3 h postprandially, on each day with breakfast and without breakfast, respectively, in every subject. Net FV after lunch did not differ between cases with and without breakfast, either in the SMA or in the CCA. Blood FV in the SMA was significantly increased after eating lunch regardless of whether breakfast was eaten (P<0·05 each). However, FV in the CCA was significantly decreased until 1 h after lunch compared with the preprandial state in cases without breakfast (P<0·05), but not in cases with breakfast. In conclusion, a sudden decrease in FV in the CCA from the preprandial state is seen after lunch when breakfast is skipped., (© 2018 Scandinavian Society of Clinical Physiology and Nuclear Medicine. Published by John Wiley & Sons Ltd.)

New Findings: What is the central question of this study? Visceral ischaemia is one of the most feared complications during use of an intra-aortic balloon pump. Using an animal model, we measured the flows at the abdominal level directly and examined flow patterns to enable investigation of flow patterns during the use of the intra-aortic balloon pump. What is the main finding and its importance? We show that there is a significant balloon-related reduction in superior mesenteric flow in both early and mid-diastole., Abstract: A number of previous studies have shown that blood flow in the visceral arteries is altered during intra-aortic balloon pump (IABP) treatment. We used a porcine model to analyse the pattern of blood flow into the visceral arteries during IABP use. For this purpose, we measured the superior mesenteric, right renal and left renal flows before and during IABP support, using surgically placed flowmeters surrounding these visceral arteries. The superior mesenteric flow significantly decreased in early diastole (P < 0.001) and in mid-diastole (P = 0.003 versus early diastole), whereas in late diastole it increased again (P < 0.001 versus mid-diastole). During systole, the flow was not significantly increased compared with late diastole (P = 0.51), but it was significantly lower than at baseline (both P < 0.001). Flows did not differ between right and left kidneys. Perfusion of either kidney did not change significantly in early diastole (P > 0.05), whereas it decreased significantly in mid-diastole (P < 0.001), rising dramatically in late diastole (P < 0.001) and with an additional slight increase in systole (P = 0.054). This study provides important insights into abdominal flows during intra-aortic pump counterpulsation. Furthermore, it supports the need to rethink the balloon design to avoid visceral ischaemia during circulatory assistance., (© 2019 The Authors. Experimental Physiology © 2019 The Physiological Society.)

Objective: To investigate the effect of caffeine infusion on superior mesenteric artery (SMA) blood flow velocities (BFV) in preterm infants., Methods: Prospective observational study on 38 preterm neonates 28-33 +6 weeks gestation, who developed apnea on their first day of life, and caffeine citrate infusion was initiated at a loading dose of 20 mg/kg, followed by a maintenance dose of 5-10 mg/kg/day. Duplex ultrasound measurements of SMA BFV were recorded: peak systolic velocity (PSV), end diastolic velocity (EDV) and resistive index (RI), at 15 min before, 1-, 2- and 6-h after caffeine loading dose, and 2 h after two maintenance doses., Results: There was a significant reduction in PSV 1-h (p = .008), a significant decrease in EDV 1- and 2-h (p = .000 and p = .005, respectively) and a significant increase in RI 1- and 2-h (p = .003 and p = .005, respectively) following caffeine loading dose, as compared to values before caffeine infusion. No significant effect of caffeine maintenance doses on SMA BFV was observed (p > .05)., Conclusion: Blood flow in SMA is significantly reduced after caffeine citrate infusion at a loading dose of 20 mg/kg. This effect continues for at least 2 h. Meanwhile, SMA BFV seems not affected by maintenance doses.

Background: Ivabradine is a funny current inhibitor which is administered to patients with congestive heart failure to reduce their heart rate (HR) and attenuate oxidative stress. Chronic liver diseases are characterized by portal hypertension and hyperdynamic circulation with tachycardia. The present study aimed to investigate the effect of ivabradine on portal hypertension., Methods: Male Sprague-Dawley rats received partial portal vein ligation (PVL) to induce portal hypertension. The PVL rats were randomly allocated to receive either vehicle or ivabradine treatment for 10 days. Then the hemodynamic data were collected. The levels of oxidative stress markers and the mRNA expression of nitric oxide synthase (NOS) were measured in the collateral vessel, the superior mesentery artery and the liver. In addition, the collateral vascular responsiveness to arginine vasopressin (AVP) was examined in the ivabradine-treated and vehicle-treated PVL rats., Results: Treatment with ivabradine significantly lowered the HR (174 ± 20 vs. 374 ± 9 beats/min; p < 0.001) and the superior mesentery arterial flow (SMAf) (6.6 ± 0.3 vs. 9.1 ± 0.7 mL/min/100 g BW; p = 0.005) of the PVL rats compared with the control group. The mean arterial pressure, cardiac index, systemic vascular resistance, portal pressure and serum levels of oxidative stress markers were not significantly affected by ivabradine treatment. In addition, the NOS expression and collateral vascular responsiveness to AVP were not significantly influenced by ivabradine treatment, either., Conclusion: Ivabradine reduced the HR and SMAf in PVL rats, which alleviated the hyperdynamic circulatory state and splanchnic hyperemia of portal hypertension. However, whether these effects would help alleviate portal hypertension-related complications requires further clinical investigations.

Upon stimulation, endothelial cells release various factors to regulate the vascular tone. In particular, vasorelaxing factors, called endothelium-derived relaxing factors (EDRFs), are altered in the production and/or release, as well as their signaling every vessel and under pathophysiological states, including cardiovascular, kidney, and metabolic diseases. Although indoxyl sulfate is known as a protein-bound uremic toxin and circulating levels are elevated in the impaired kidney functions, direct impact on the vascular function, especially EDRF's signaling, remains unclear. In this study, we hypothesize that acute exposure to indoxyl sulfate could alter vascular relaxation in the rat superior mesenteric artery. Accordingly, we measured acetylcholine (ACh)-induced endothelium-dependent relaxation in the absence and presence of several inhibitors to divide into each EDRF, including nitric oxide (NO), vasodilator prostaglandins (PGs), and endothelium-derived hyperpolarizing factor (EDHF). Indoxyl sulfate reduced the sensitivity to ACh but not sodium nitroprusside. Under cyclooxygenase (COX) inhibition or inhibitions of COX plus source of EDHF, such as small (SK Ca )- and intermediate (IK Ca )-conductance calcium-activated K + channels, the decreased sensitivity to ACh in indoxyl sulfate exposed vessel was still preserved. However, under inhibition of NO synthase (NOS) or inhibitions of NOS and COX, the difference of sensitivity to ACh between vehicle and indoxyl sulfate was eliminated. These findings indicated that acute exposure of indoxyl sulfate in the rat superior mesenteric artery specifically explicitly impaired NO signaling but not EDHF or vasodilator PGs.

Objectives: The objective of this study is to evaluate intestinal blood flow changes within the first 72 h in the late preterm infants in comparison with the healthy term neonates., Methods: In this prospective study, we analyzed Doppler flow velocity waveforms of superior mesenteric artery (SMA) and coeliac trunc (TC) in 20 late preterm and 20 term infants at the age of 2, 24, and 72 h., Results: Significant end-diastolic velocity (end-diastolic velocity (EDV) SMA ) rise up to 24 h was documented in all patients (late preterm: -9.32 ± 9.48 to 17.01 ± 6.94; p < .05; term: -8 ± 5.74 to 12.39 ± 3.33; p < .001), associated with a conversion from negative values to positive ones. Reversed blood flow was documented in SMA at 2 h in 75% late preterm neonates. Preterm infants showed significantly higher mean peak systolic velocities (peak systolic velocity (PSV) SMA ), end-diastolic velocities (EDV SMA ) at 24 h and PSV TC at 72 h than term infants (p < .05). The resistance and pulsatility indices (PI) decreased within 24 h in both groups and inversely reflected the postnatal changes in EDV SMA . Mean PI AMS at 2 h was significantly higher in term neonates., Conclusion: Late preterm neonates show similar progressive postnatal increase in blood flow velocities accompanied with a decrease in vascular resistance in SMA and TC then term neonates.

Aims: Royal jelly (RJ) has a variety of reported biological activities, including vasorelaxation and blood pressure-lowering effects. Although functional foods are positively used for health, the effects of RJ on the cardiovascular system in healthy individuals have not been well studied. Therefore, we investigated the mechanisms underlying the vasorelaxation effects of RJ in healthy control rats to evaluate whether the peripheral circulation was increased., Main Methods: We used fresh RJ to examine the vasorelaxation effects and related mechanisms in Wistar rats using organ bath techniques. Furthermore, we measured changes in tail blood circulation, systolic blood pressure (sBP), and heart rate (HR) after the oral administration of RJ to control rats and nitro-l-arginine methyl ester (l-NAME)-treated rats (0.5 mg/ml dissolved in distilled drinking water for 1 week). Concentrations of acetylcholine (ACh) in the RJ were measured using a commercial kit., Key Findings: RJ caused vasorelaxation of isolated rat aortas and superior mesenteric arteries, and this effect was inhibited by atropine (10 -5 M, 15 min) or L-NAME (10 -4 M, 20 min) and endothelium-denuded arterial ring preparations. Oral RJ increased tail blood flow and mass in control rats 1 h after treatment without affecting velocity, sBP, or HR. These effects were not observed in L-NAME-treated rats. RJ contained approximately 1000 μg/g of ACh., Significance: The present study demonstrated that RJ is composed of muscarinic receptor agonist(s), likely ACh, and induces vasorelaxation through nitric oxide (NO) production from the vascular endothelium of healthy rats, leading to increased tail blood circulation. Thus, fresh RJ may improve peripheral circulation in healthy individuals., (Copyright © 2018 Elsevier Masson SAS. All rights reserved.)

Transplanted Intestinal Segments (IS) must match the perfusion capacities of the recipient. This can be challenging during a size-mismatched SBTX. In this study, we defined the maximum IS length with lowest blood flow needs in a porcine model by evaluating the physiological perfusion rates of different IS lengths. Blood flow in the SMA, aorta segment four, and general circulatory parameters were monitored before and after sequential intestinal resection. IS lengths of 30 cm, 60 cm, 120 cm, and 300 cm (n = 8 each) were compared. The IS blood flow requirements increased with IS length (30 cm: 19.5 ± 3.4 mL/min; 60 cm: 16.9 ± 6.7 mL/min; 120 cm: 34.9 ± 8.5 mL/min; 300 cm: 62.9 ± 11.6 mL/min). Absolute IS blood flow (P = .004), percentage IS blood flow uptake from the SMA (P = .001), and percentage IS blood flow uptake from the aorta (P = .005) increased significantly between 60 cm and 120 cm. We concluded that 60 cm was the maximum IS length before blood flow demands significantly increased in a porcine model., (© 2018 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Aims and Objectives: To prove the effects of an enteral feeding improvement massage for premature infants with regard to their feeding, growing and superior mesentery artery blood flow aspect by a randomised controlled trial., Background: Premature infants have feeding-related problems related to eating and absorbing nutrition due to their immature gastrointestinal function. Studies regarding the effectiveness of premature infants' enteral feeding improvement by tactile stimulation massage are rare., Design: The study group was composed of 55 patients. Of the 55 patients, 26 were randomised into an experimental group and 29 were randomised into a control group., Methods: They were all born <34 weeks of gestational age between 1 July 2011 and 30 March 2012. Premature infants in the experimental group received enteral feeding improvement massage twice a day for 14 days, and infants in the control group received a sham exercise. The collected data were analysed by spss 19.0, through t test, chi-square test (Fisher's exact) and ANCOVA., Results: (i) The experimental group had reached the day of full enteral feeding significantly faster. (ii) The experimental group had a higher superior mesentery artery peak velocity (V max ) and lower RI (resistant index). (iii) The experimental group of the feeding-intolerant subgroup had a higher superior mesentery artery V max and V min . (iv) The experimental group had a heavier weight and larger head circumference after 14 days., Conclusions: This study demonstrates that enteral feeding improvement massage can be helpful for achieving earlier full enteral feeding, more increased superior mesentery artery, and faster growing. In particular, it can be a therapeutic, independent and evidence-based nursing intervention for feeding-intolerant premature infants., Relevance to Clinical Practice: Neonatal nurses in neonatal intensive care unit can apply enteral feeding improvement massage massage for feeding-intolerant infants., (© 2017 John Wiley & Sons Ltd.)

Endothelium-derived hyperpolarization (EDH) is an important signaling mechanism of endothelium-dependent vasorelaxation, and little attention has been paid to the EDH-type responses in female metabolic syndrome such as that observed with type-2 diabetes. We previously reported that EDH-type relaxation was impaired in superior mesenteric arteries from male Otsuka Long-Evans Tokushima Fatty (OLETF) rat, a model of type-2 diabetes, however, the response was unclear in female OLETF rat. Thus, the aim of this study was to examine if EDH-type relaxation was altered in superior mesenteric arteries isolated from female OLETF rats compared to age-matched, control female Long-Evans Tokushima Otsuka (LETO) rats at age 50-59 weeks. We investigated concentration-relaxation curves for acetylcholine (at age 50-53 weeks), NS309 (an activator of small- and intermediate-conductance calcium-activated potassium channels) (at age 50-53 weeks), and GSK1016790A (an agonist of transient receptor potential vanilloid type 4, TRPV4) (at age 58 or 59 weeks) in the presence of the nitric oxide synthase inhibitor N G -nitro-L-arginine and the cyclooxygenase inhibitor indomethacin to investigate EDH-type responses in the superior mesenteric artery. Obesity, mild hyperglycemia, hyperinsulinemia, and hyperlipidemia (i.e., increased total cholesterol, triglyceride, and non-esterified fatty acids) were more frequent in OLETF rats than in age-matched LETO rats at age 50-53 weeks. Acetylcholine-, NS309-, and GSK1016790A-induced relaxations in arteries from OLETF rats were all significantly reduced compared to those in LETO rats. These results indicated that EDH-type relaxations were impaired in female OLETF rats. This novel experimental model may provide new insights into vascular dysfunction in metabolic syndrome in females., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Aim: We evaluated the influence of intra-aortic balloon size and volume on mesenteric and renal flows., Methods: Thirty healthy swine underwent 120-minute ligation of the left anterior descending coronary artery followed by 6 hours of reperfusion. Then, they were randomly assigned to the following five groups of animals, with six animals in each group: no intra-aortic balloon pump (IABP), a short 35-mL IABP, a short 40-mL IABP, a long 35-mL IABP and a long 40-mL IABP. Superior mesenteric artery (SMA) and renal flows were measured at baseline (t 0 ), at 2-hour ischemia (t 1 ) and every hour thereafter until 6 hours of reperfusion (from t R1 to t R6 )., Results: SMA flows increased significantly at t R1 only in the two short IABP groups (p<0.001) and balloon volume did not appear to affect flows which, at any experimental time-point, were comparable using 35 mL or 40 mL balloons (p>0.05). Renal flows appeared to be influenced by balloon length, but not by volume. Indeed, flows in the renal arteries rose during IABP treatment; the increase was significantly higher in the short balloon groups and throughout the whole reperfusion (all, p<0.001)., Conclusions: Changes in visceral perfusion during IABP assistance were significantly related to balloon length, but not to its volume. This could be relevant for the evolution of balloon engineering design in order to reduce the incidence of mesenteric ischemia following IABP. Further research is necessary to confirm these findings.

The adipokine chemerin causes arterial contraction and is implicated in blood pressure regulation, especially in obese subjects with elevated levels of circulating chemerin. Because chemerin is expressed in the perivascular adipose tissue (PVAT) that surrounds the sympathetic innervation of the blood vessel, we tested the hypothesis that chemerin (endogenous and exogenous) amplifies the sympathetic nervous system in mediating electrical field-stimulated (EFS) contraction. The superior mesenteric artery, with or without PVAT and with endothelium and sympathetic nerve intact, was mounted into isolated tissue baths and used for isometric contraction and stimulation. Immunohistochemistry validated a robust expression of chemerin in the PVAT surrounding the superior mesenteric artery. EFS (0.3-20 Hz) caused a frequency-dependent contraction in isolated arteries that was reduced by the chemerin receptor ChemR23 antagonist CCX832 alone (100 nM; with, but not without, PVAT), but not by the inactive congener CCX826 (100 nM). Exogenous chemerin-9 (1 μM)-amplified EFS-induced contraction in arteries (with and without PVAT) was blocked by CCX832 and the α-adrenergic receptor antagonist prazosin. CCX832 did not directly inhibit, nor did chemerin directly amplify, norepinephrine-induced contraction. Whole mount immunohistochemical experiments support colocalization of ChemR23 with the sympathetic nerve marker tyrosine hydroxylase in superior mesenteric PVAT and, to a lesser extent, in arteries and veins. These studies support the idea that exogenous chemerin modifies sympathetic nerve-mediated contraction through ChemR23 and that ChemR23 may be endogenously activated. This is significant because of the well-appreciated role of the sympathetic nervous system in blood pressure control., (Copyright © 2016 the American Physiological Society.)

Background: Abdominal complications being rare but results in high mortality, commonly due to splanchnic organ hypoperfusion during the perioperative period of cardiac surgery. There are no feasible methods to monitor intraoperative superior mesenteric artery blood flow (SMABF). Hence, the aim of this study was to evaluate the feasibility and to measure SMABF using transesophageal echocardiography (TEE) during cardiac surgery under hypothermic cardiopulmonary bypass (CPB)., Methodology: Thirty-five patients undergoing elective cardiac surgery under CPB were enrolled. Heart rate, mean arterial pressure (MAP), cardiac output (CO), SMABF, superior mesenteric artery (SMA) diameter, superior mesentric artery blood flow over cardiac output (SMA/CO) ratio and arterial blood lactates were recorded at three time intervals. T0: before sternotomy, T1: 30 min after initiation of CPB and T2: after sternal closure., Results: SMA was demonstrated in 32 patients. SMABF, SMA diameter, SMA/CO, MAP and CO-decreased significantly (P < 0.0001) between T0 and T1, increased significantly ( P ≤ 0.001) between T1 and T2 and no significant change (P > 0.05) between T0 and T2. Lactates increased progressively from T0 to T2., Conclusion: Study shows that there is decrease in SMABF during CPB and returns to baseline after CPB. Hence, it is feasible to measure SMABF using TEE in patients undergoing cardiac surgery under hypothermic CPB. TEE can be a promising tool in detecting and preventing splanchnic hypoperfusion during perioperative period.

Objective: We aimed to demonstrate the effect of continuous or bolus nasogastric feeding on gastric emptying, small bowel water content, and splanchnic blood flow measured by magnetic resonance imaging (MRI) in the context of changes in plasma gastrointestinal hormone secretion., Background: Nasogastric/nasoenteral tube feeding is often complicated by diarrhea but the contribution of feeding strategy to the etiology is unclear., Methods: Twelve healthy adult male participants who underwent nasogastric intubation before a baseline MRI scan, received 400  mL of Resource Energy (Nestle) as a bolus over 5 minutes or continuously over 4  hours via pump in this randomized crossover study. Changes in gastric volume, small bowel water content, and superior mesenteric artery blood flow and velocity were measured over 4  hours using MRI and blood glucose and plasma concentrations of insulin, peptide YY, and ghrelin were assayed every 30 minutes., Results: Bolus nasogastric feeding led to significant elevations in gastric volume (P < 0.0001), superior mesenteric artery blood flow (P < 0.0001), and velocity (P = 0.0011) compared with continuous feeding. Both types of feeding reduced small bowel water content, although there was an increase in small bowel water content with bolus feeding after 90 minutes (P < 0.0068). Similarly, both types of feeding led to a fall in plasma ghrelin concentration although this fall was greater with bolus feeding (P < 0.0001). Bolus feeding also led to an increase in concentrations of insulin (P = 0.0024) and peptide YY (P < 0.0001), not seen with continuous feeding., Conclusion: Continuous nasogastric feeding does not increase small bowel water content, thus fluid flux within the small bowel is not a major contributor to the etiology of tube feeding-related diarrhea.

We investigated superior mesenteric arteries from spontaneously hypertensive rats (SHR) to determine the relaxation responses induced by ATP, ADP, and adenosine and the relationship between the relaxant effects of these compounds and nitric oxide (NO) or cyclooxygenase (COX)-derived prostanoids. In rat superior mesenteric artery, relaxation induced by ATP and ADP but not by adenosine was completely eliminated by endothelial denudation. In the superior mesenteric arteries isolated from SHR [vs. age-matched control Wistar Kyoto rats (WKY)], a) ATP- and ADP-induced relaxations were weaker, whereas adenosine-induced relaxation was similar in both groups, b) ATP- and ADP-induced relaxations were substantially and partly reduced by N(G)-nitro-L-arginine [a NO synthase (NOS) inhibitor], respectively, c) indomethacin, an inhibitor of COX, increased ATP- and ADP-induced relaxations, d) ADP-induced relaxation was weaker under combined inhibition by NOS and COX, and e) adenosine-induced relaxation was not altered by treatment with these inhibitors. These data indicate that levels of responsiveness to these nucleotides/adenosine vary in the superior mesenteric arteries from SHR and WKY and are differentially modulated by NO and COX-derived prostanoids.

In cellular events, endoplasmic reticulum (ER) stress has an important role in the development of various diseases including cardiovascular diseases. Tunicamycin, an inhibitor of N-linked glycosylation, is known to be an inducer of ER stress. However, the extent to which tunicamycin affects the vasorelaxant function is not completely understood. Thus, we investigated the effect of tunicamycin on relaxations induced by various vasorelaxant agents, including acetylcholine (ACh; endothelium-dependent vasodilator), sodium nitroprusside (SNP; endothelium-independent vasodilator), isoprenaline (ISO; beta-adrenoceptor agonist), forskolin (FSK; adenylyl cyclase activator), and cromakalim [ATP-sensitive K(+) (KATP) channel activator] in organ-cultured superior mesenteric arteries of rats, which are treated with either a vehicle [dimethyl sulfoxide (DMSO)] or tunicamycin (20 µg/mL for 22-24 h). Protein levels of the ER stress marker binding immunoglobulin protein (BiP) were determined by Western blotting. Tunicamycin increased the expression of BiP in organ-cultured arteries. Tunicamycin impaired ACh-induced relaxation, but did not alter SNP-induced relaxation. Tunicamycin also impaired vasorelaxation induced by ISO, FSK, and cromakalim; moreover, it reduced basal nitric oxide (NO) formation. In conclusion, short-term treatment with tunicamycin not only caused endothelial dysfunction but also impaired cAMP- and KATP-mediated responses in the superior mesenteric arteries of rats. These alterations in tunicamycin-treated arteries may be due to reduced basal NO formation. This work provides new insight into ER stress in vascular dysfunction.

Objective: The aim of the study was a comprehensive examination of the circulation of superior mesenteric artery in different weeks of pregnancy using Doppler ultrasound examination., Methods: The study was conducted at the Clinic of Obstetrics and Gynecology, Jessenius Faculty of Medicine, Comenius University, Slovakia between the years 2008 and 2012. Dynamics and changes in superior mesenteric artery circulation were studied in 856 women. Results of Doppler examination were processed and subsequently evaluated for each gestational week separately., Results: We found that changes in resistance index of superior mesenteric artery are slower and have a tendency to decrease as a consequence of a gradual decrease in vascular resistance. The changes in pulsatility index are different in nature; there is a tendency for there are to be repeating periods of higher and then lower values, which are subject to a more pronounced dependence on flow rate, especially end diastolic velocity, and Vmean., Conclusions: This article and its results bring a new, comprehensive view not only of physiological changes in the splanchnic circulation, but also of changes that may be subject to a certain extent, not only to the sex, but primarily to the weight of the fetus, which, of course, indirectly reflects its metabolic and respiratory demands.

Objective: To describe and to characterize the relaxing effect of an extract of the bark of Combretum leprosum on isolated arterial rings from different animals., Methods: Rings (3 to 4mm) from rabbit, rat, or porcine arteries rings were suspended in an organ bath (Krebs, 37°C, 95%O2/5%CO2) to record isometric contractions. After the stabilization period (2 to 3 hours) contractions were induced by the addition of phenylephrine (0.1 to 0.3µM) or U46619 (10 to 100nM), and Combretum leprosum extract was added on the plateau of the contractions. Experiments were performed to determine the potency, duration, reversibility, and to get insights on the potential mechanism involved in extract-induced relaxations., Results: In all rings tested, Combretumleprosum extract (1.5μg/mL) was able to cause relaxations, which were strictly endothelium-dependent. In rabbit or rat thoracic aorta rings, the relaxations were reversed by vitamin B12a or L-NG-nitroarginine. In porcine right coronary arteries and rabbit abdominal aorta, extract caused both L-NG-nitroarginine-sensitive and L-NG-nitroarginine-resistant relaxations. In rabbit thoracic aorta, the extract was relatively potent (EC50=0.20µg/mL) and caused relaxations; intriguingly the endothelium continued to produce relaxing factors for a long period after removing the extract. The magnitude of extract-induced relaxations was significantly reduced in the absence of extracellular Ca2+; in addition, the TRPs channels blocker ruthenium red (10µM) was able to revert extract-induced relaxations. Phytochemical analyses indicated that the extract was rich in polyphenol-like reacting substances., Conclusions: Combretum leprosum extract contains bioactive compounds capable of promoting Ca2+-dependent stimulation of endothelial cells which results in a prolonged production of relaxing factors.

Objectives: To evaluate intestinal blood flow changes after intravenous immunoglobulin (IVIg) infusion among neonates with Rh isoimmunization and alloimmune thrombocytopenia., Methods: This prospective observational study was conducted in level III NICU from July 2011 through August 2012. Thirty three consecutive instances (30 neonates) of IVIg treatment (1 g/kg) were studied. Celiac (CA) and superior mesenteric artery (SMA) doppler evaluations were performed immediately prior (baseline), immediately after and 12 to18 h following IVIg infusion. Peak systolic velocity, end diastolic velocity, time-averaged mean velocity, pulsatility index, resistive index and systolic/diastolic ratio were measured. The doppler indices measured immediately after and 12 to 18 h after IVIg infusion were compared with the baseline values., Results: The mean gestation and birth weight of the cohort were 36 ± 2 wk and 2597 ± 563 g respectively. Doppler flow variables measured immediately after and 12 to 18 h after IVIg were comparable to baseline values, in both the arteries. However, systolic/diastolic ratio in SMA immediately post-IVIg was lower than baseline, [median (IQR): 5 (3, 9) vs. 7 (4, 14), respectively; p=0.02]. None of the study infants developed feed intolerance or necrotizing enterocolitis (NEC)., Conclusions: There was no significant change in the celiac and SMA blood flows following IVIg therapy in neonates with Rh isoimmunization and alloimmune thrombocytopenia.

Purpose: To investigate the feasibility of selective arterial and portal venous liver perfusion imaging with spin labelling (SL) MRI, allowing separate labelling of each blood supply., Methods: The portal venous perfusion was assessed with a pulsed EPISTAR technique and the arterial perfusion with a pseudo-continuous sequence. To explore precision and reproducibility, portal venous and arterial perfusion were separately quantified in 12 healthy volunteers pre- and postprandially (before and after meal intake). In a subgroup of 6 volunteers, the accuracy of the absolute portal perfusion and its relative postprandial change were compared with MRI flow measurements of the portal vein., Results: The portal venous perfusion significantly increased from 63 ± 22 ml/100g/min preprandially to 132 ± 42 ml/100g/min postprandially. The arterial perfusion was lower with 35 ± 22 preprandially and 22 ± 30 ml/100g/min postprandially. The pre- and postprandial portal perfusion using SL correlated well with flow-based perfusion (r(2) = 0.71). Moreover, postprandial perfusion change correlated well between SL- and flow-based quantification (r(2) = 0.77). The SL results are in range with literature values., Conclusion: Selective spin labelling MRI of the portal venous and arterial blood supply successfully quantified liver perfusion. This non-invasive technique provides specific arterial and portal venous perfusion imaging and could benefit clinical settings where contrast agents are contraindicated., Key Points: • Perfusion imaging of the liver by Spin Labelling MRI is feasible • Selective Spin Labelling MRI assessed portal venous and arterial liver perfusion separately • Spin Labelling based portal venous liver perfusion showed significant postprandial increase • Spin Labelling based portal perfusion correlated well with phase-contrast based portal perfusion • This non-invasive technique could benefit settings where contrast agents are contraindicated.

Infusion of 5-hydroxytryptamine (5-HT) in conscious rats results in a sustained (up to 30 days) fall in blood pressure. This is accompanied by an increase in splanchnic blood flow. Because the splanchnic circulation is regulated by the sympathetic nervous system, we hypothesized that 5-HT would: 1) directly reduce sympathetic nerve activity in the splanchnic region; and/or 2) inhibit sympathetic neuroeffector function in splanchnic blood vessels. Moreover, removal of the sympathetic innervation of the splanchnic circulation (celiac ganglionectomy) would reduce 5-HT-induced hypotension. In anaesthetized Sprague-Dawley rats, mean blood pressure was reduced from 101±4 to 63±3mm Hg during slow infusion of 5-HT (25μg/kg/min, i.v.). Pre- and postganglionic splanchnic sympathetic nerve activity were unaffected during 5-HT infusion. In superior mesenteric arterial rings prepared for electrical field stimulation, neither 5-HT (3, 10, 30nM), the 5-HT1B receptor agonist CP 93129 nor 5-HT1/7 receptor agonist 5-carboxamidotryptamine inhibited neurogenic contraction compared to vehicle. 5-HT did not inhibit neurogenic contraction in superior mesenteric venous rings. Finally, celiac ganglionectomy did not modify the magnitude of fall or time course of 5-HT-induced hypotension when compared to animals receiving sham ganglionectomy. We conclude it is unlikely 5-HT interacts with the sympathetic nervous system at the level of the splanchnic preganglionic or postganglionic nerve, as well as at the neuroeffector junction, to reduce blood pressure. These important studies allow us to rule out a direct interaction of 5-HT with the splanchnic sympathetic nervous system as a cause of the 5-HT-induced fall in blood pressure., (Copyright © 2015 Elsevier B.V. All rights reserved.)

Background: Previous studies have shown that aqueous extract of the leaf of Tridax procuinbens is capable of lowering blood pressure through its vasodilatory effects. In the present study attempt was made to examine the biological active components of T procuinbens leaf using GC-MS methods. We further investigated the role of K+ channels in the vasorelaxation effects of Tridax procumbens using rat isolated mesenteric artery., Methods: The superior mesenteric artery isolated from healthy, young adult Wistar rats (250-300 g) were precontracted with phenylephrine (PE) (10(-7) M) and potassium chloride (KCl) (60 mM) and were treated with Various concentrations of aqueous extract ofT procumbens (0.9.0 mg/ml). The changes in arterial tension were recorded using a force-displacement transducer (Model 7004; Ugo Basil Varese, Italy) coupled to data capsule acquisition system., Results: The results of GG-MS revealed the presence of linoleic acid. The T. procumbens extract (TPE) ranging from 0.5-9.0 mg/mI significantly (p<0.05) reduced the, contraction induced by (PE) and (KCl) in a concentration-dependent manner. The extract also antagonised the calcium-induced vasoconstriction (1(-9) - 10(-5)) in calcium-free with high concentration of potassium as well as. in calcium- and potassium free physiological solutions. The vasorelaxing effect caused by TPE was significantly (p<0.05) attenuated with preincubation of potassium channels blockers (Barium chloride and apamin), NO synthaseinhibitor (L-NAME), prostacyclin inhibitor (indomethacin), atropine; propranolol, and methylene blue while it was not affected by preincubation with glibenclamide and tetra ethyl ammonium, 4-aminopyridine (4-AP) and oxadiazolo quinoxalin (ODQ)., Conclusion: The results of this study demonstrate that T procumbens extract causes vasodilatory effects by blocking calcium channels and the vasodilatory effect of the extract may also be due to stimulation of prostacyclin production and opening of small-conductance Ga2+ activated potassium channels. The observed effect of this extract may be probably due to the presence of linoleic acid in this extract.

Objective: To determine whether packed red blood cell (PRBC) transfusion affects post-prandial superior mesenteric artery blood flow velocities (SMA BFVs) in very-low birth weight (VLBW) neonates and if so, at what time point after transfusion restoration of previous SMA BFV patterns occurs., Design/methods: VLBW pre-term neonates, older than 14 days and tolerating bolus enteral feedings administered every 3 h were enrolled in this prospective observational study. Pulsed Doppler ultrasound was used to measure pre- and post-prandial (at 45 min) time-averaged mean, peak and end diastolic velocities (TAMV, PSV, EDV) immediately before and after 15 ml/kg of PRBC transfusion was given over 3 h; patent ductus arteriosus (PDA) status was also evaluated. Subsequent pre- and post-prandial SMA BFVs were recorded 24 and 48 h after the transfusion., Results: Pre- and post-prandial measurements were obtained for 21 out of 25 enrolled infants. Post-prandial SMA BFVs were attenuated during the feedings immediately after transfusion; at 24 and 48 h after transfusion, changes in post-prandial SMA BFVs were similar to those measured prior to transfusion; the presence of the PDA did not affect results., Conclusions: PRBC transfusion blunted SMA BFV responses to feedings immediately after the transfusion with normalization observed 24 h post-transfusion.

Background: Hypertension is considered an independent risk factor for cardiovascular mortality in diabetic patients. The present study was designed to determine the role of gamma amino butyric acid B (GABAB) receptor and L-arginine (L-Arg) in GABA-induced vasorelaxation in normal and streptozotocin-induced diabetic rat vessels., Methods: Diabetes was induced by a single i.p. injection of streptozotocin (STZ, 60 mg/kg). Eight weeks later, superior mesenteric arteries of all groups were isolated and perfused according to the McGregor method., Results: Baseline perfusion pressure of STZ diabetic rats was significantly higher than non-diabetic rats in both intact and denuded endothelium. In the presence of faclofen, a selective GABAB receptor blocker, GABA-induced relaxation in intact and denuded endothelium mesenteric beds of STZ diabetic rats was suppressed, but this response in non-diabetic rats was not suppressed. Our results showed that in the presence of L-Arg, a nitric oxide precursor, GABA induced vasorelaxation in both diabetic and non-diabetic vessels., Conclusion: From the results of this study, it may be concluded that the vasorelaxatory effect of GABA in diabetic vessel is mediated by the GABAB receptor and nitric oxide, but it seems that in non-diabetic vessel GABAB receptor does not play any role in GABA-induced vasorelaxation, but nitric oxide induced GABA relaxation in non-diabetic vessel.

Purpose: To evaluate the safety and efficacy of coil embolization with an indwelling catheter with side holes to control visceral artery bleeding while simultaneously preserving peripheral artery flow., Materials and Methods: A 6-F anticoagulant-coated catheter with two symmetrically arranged side holes was used with coil embolization to induce hemostasis in the superior mesenteric artery (SMA) of 13 pigs. The SMA was punctured with a metal needle to induce bleeding. The catheter was advanced into the SMA immediately after the puncture, and the midpoint between its tip and side holes was adjusted to conform to the puncture site. The SMA was embolized by using microcoils placed around the catheter to achieve hemostasis. Hemostasis and gross ischemic changes of the intestine were visually observed during the abdominal surgery. Peripheral blood flow was assessed by using abdominal aortography for as long as 2 hours in 13 pigs and was assessed again at 7 days in three pigs., Results: Antegrade peripheral artery flow through the indwelling catheter was preserved without stagnation for as long as 2 hours in all 13 pigs and at 7 days in two of three pigs. One catheter occlusion was seen at the 7-day time point. There were no observable instances of recurrent bleeding, ischemic changes in the intestine, or vascular adverse events during or after the procedure., Conclusions: The hemostatic method described here is a technically feasible method of controlling acute visceral artery bleeding while preserving peripheral artery flow and may be particularly useful in cases of absence of collateral circulation. Further experiments are warranted for clinical application., (Copyright © 2014 SIR. Published by Elsevier Inc. All rights reserved.)

Objective: Near-infrared spectroscopy is a noninvasive method of measuring local tissue oxygenation (StO2). Abdominal StO2 measurements in preterm piglets are directly correlated with changes in intestinal blood flow and markedly reduced by necrotizing enterocolitis. The objectives of this study were to use near-infrared spectroscopy to establish normal values for abdominal StO2 in preterm infants and test whether these values are reduced in infants who develop necrotizing enterocolitis., Design: We conducted a 2-year prospective cohort study where we prospectively measured abdominal StO2 in preterm infants, to establish reference values for preterm infants, and compared the near-infrared spectroscopy values with preterm infants in the cohort that developed necrotizing enterocolitis., Setting: Two neonatal ICUs: one at Texas Children's Hospital and the other at Ben Taub General Hospital in Houston, TX., Patients: We enrolled 100 preterm infants (< 32 weeks' gestation and < 1,500 g birth weight) between January 2007 and November 2008., Interventions: None., Measurements and Main Results: Eight neonates with incomplete data were excluded. Mean abdominal StO2 in normal preterm infants (n = 78) during the first week of life was significantly higher than in those who later developed necrotizing enterocolitis (n = 14) (77.3% ± 14.4% vs 70.7% ± 19.1%, respectively, p = 0.002). An StO2 less than or equal to 56% identified preterm infants progressing to necrotizing enterocolitis with 86% sensitivity, 64% specificity, 96% negative predictive value, and 30% positive predictive value. Using logistic regression, StO2 less than or equal to 56% was independently associated with a significantly increased risk of necrotizing enterocolitis (odds ratio, 14.1; p = 0.01). Furthermore, infants with necrotizing enterocolitis demonstrated significantly more variation in StO2 both during and after feeding in the first 2 weeks of life., Conclusions: This study establishes normal values for abdominal StO2 in preterm infants and demonstrates decreased values and increased variability in those with necrotizing enterocolitis. Abdominal near-infrared spectroscopy monitoring of preterm infants may be a useful tool for early diagnosis and guiding treatment of necrotizing enterocolitis.

Experiments on anesthetized rats carried out with a high-frequency ultrasonic system and tropicamide, a highly selective blocker of M4 cholinoreceptors, showed that the vasodilator effects observed after selective blockade of M4 cholinoreceptors are not organ-specific. Intravenous tropicamide (0.1 μg/kg body weight) transiently decreased systemic BP, elevated the linear and volume fl ow rates, and diminished vascular resistance in common carotid, superior mesenteric, and femoral arteries. At the same time, in most rats (76%) the fl ow rate in the portal vein did not change, while in 25% rats it insignificantly and temporarily increased. The hypothesis on possible involvement of M4 cholinoreceptor structures in cholinergic vasoconstriction is discussed.

Background: Activated macrophage infiltration into the lungs is paramount in the pathogenesis of acute lung injury (ALI) induced by intestinal ischemia-reperfusion (I/R). Omega-3 polyunsaturated fatty acid (ω-3 PUFA) is a potent activator of the Adenosine 5'-monophosphate-activated protein kinase-sirtuin1 (AMPK/SIRT1) pathway against macrophage inflammation. We aimed to evaluate whether ω-3 PUFAs may protect against ALI induced by intestinal I/R via the AMPK/SIRT1 pathway., Methods: Ischemia in male Wistar rats was induced by superior mesenteric artery occlusion for 60 min and reperfusion for 240 min. One milliliter per day of fish-oil emulsion (FO emulsion, containing major ingredients as ω-3 PUFAs) or normal saline (control) was administered by intraperitoneal injection for three consecutive days to each animal. All animals were sacrificed at the end of reperfusion. Blood and tissue samples were collected for analysis., Results: Intestinal I/R caused intestinal and lung injury, evidenced by severe lung tissue edema and macrophage infiltration. Pretreatment with FO emulsion improved the integrity of microscopic structures in the intestine and lungs. Intestinal I/R induced the expression of macrophage-derived mediators (macrophage migration inhibitory factor and macrophage chemoattractant protein-1), inflammatory factors (nuclear factor κB, tumor necrosis factor α, interleukin 6, and interleukin 1β), and proapoptosis factor p66shc. There was a decrease in the expression of AMPK, SIRT1, and claudin 5. FO emulsion significantly inhibited macrophage infiltration into the lungs, inflammatory factor expression, and p66shc phosphorylation. Importantly, FO emulsion restored AMPK, SIRT1, and claudin 5 in the lungs., Conclusions: Pretreatment with ω-3 PUFAs effectively protects intestinal and lung injury induced by intestinal I/R, reduces macrophage infiltration, suppresses inflammation, inhibits lung apoptosis, and improves the lung endothelial barrier after intestinal I/R in a manner dependent on AMPK/SIRT1. Thus, there is a potential for developing AMPK/SIRT1 as a novel target for patients with intestinal I/R-induced ALI., (Copyright © 2014 Elsevier Inc. All rights reserved.)

We examined superior mesenteric artery blood flow velocity in response to feeding in infants randomized to trophic feeds (n = 16) or nil per os (n = 18) during previous treatment for patent ductus arteriosus. Blood flow velocity increased earlier in the fed infants, but was similar in the 2 groups at 30 minutes after feeding., (Copyright © 2014 Mosby, Inc. All rights reserved.)

Background: Resveratrol has been shown to attenuate reactive oxygen species formation and protect against ischemia-reperfusion (I/R) injury. However, the effects of resveratrol against subacute intestinal I/R injury are not clearly elucidated. Therefore, this study was designed to investigate the effects and possible protective mechanisms of resveratrol on subacute intestinal I/R injury in mice., Methods: BALB/c mice were subjected to 1 h ischemia by occluding the superior mesenteric artery and 24 h reperfusion. Histologic injury; myeloperoxidase, superoxide dismutase, and glutathione peroxidase activity; malondialdehyde level; inducible nitric oxide synthase (iNOS), Ac-NF-κBp65, and sirtuin 1 (SIRT1) expression; NF-κB translocation; and nitric oxide (NO) production were examined in treated with or without resveratrol in the absence or presence of pharmacologic inhibitors., Results: Resveratrol significantly ameliorated subacute intestinal I/R injury accompanied with the decrease of NO production as well as iNOS expression. In addition, resveratrol obviously upregulated the expression of SIRT1 and inhibited the activity of NF-κB. After application of iNOS inhibitor S-methylisothiourea and NF-κB inhibitor pyrrolidine dithiocarbamate, the protective effect of resveratrol was significantly augmented by attenuating iNOS and NO production, indicating that resveratrol exerted its protective effect on intestinal I/R injury via NF-κB-mediated iNOS pathway. Furthermore, the protective effect of resveratrol was correlated with SIRT1, because application of SIRT1 inhibitor nicotinamide strikingly weakened the protective effect of resveratrol., Conclusions: Taken together, our findings showed that resveratrol protects intestinal subacute I/R injury via the SIRT1-NF-κB pathway in an iNOS-NO-dependent manner. Therefore, resveratrol has a potential clinical prospect for further development of anti-injury therapy., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Background: Previous studies have demonstrated differences among organs in terms of shock-induced vascular reactivity and a role for adenosine A2A receptors (A2ARs) in protection against ischemia/reperfusion injury. However, the contributions of A2ARs to organ-specific vascular reactivity and the protection of vascular responsiveness following shock are currently unknown., Methods: We investigated the role of A2ARs in different arteries, including the left femoral artery (LFA), thoracic aorta (TA), superior mesenteric artery (SMA), right renal artery (RRA), pulmonary artery (PA), and middle cerebral artery (MCA), in hemorrhagic-shock rats., Results: The vascular reactivities of the LFA, SMA, RRA, and MCA increased slightly during early shock and then gradually decreased, whereas those of the PA and TA decreased from the start of shock. Different blood vessels lost vascular reactivity at different rates compared with controls; the LFA had the highest rate of loss (64.51%), followed by the SMA (44.69%), TA (36.06%), PA (37.83%), and RRA (32.33%), whereas the MCA had the lowest rate (18.45%). The rate of loss of vascular reactivity in the different vessels was negatively correlated with A2AR expression levels in normal and shock conditions. The highly selective A2AR agonist CGS 21680 significantly improved vascular reactivity, hemodynamic parameters, and animal survival, whereas the specific antagonist SCH58261 further decreased the shock-induced reduction in vascular reactivity and hemodynamic parameters., Conclusions: A2ARs are involved in the regulation and protection of vascular reactivity following shock. A2AR activation may have a beneficial effect on hemorrhagic shock by improving vascular reactivity and hemodynamic parameters., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Objective: Near-infrared spectroscopy (NIRS) is used to monitor brain and kidney perfusion in at-risk premature and term neonates. Although NIRS holds potential for bedside monitoring of intestinal perfusion, there is insufficient evidence showing correlation with mesenteric blood flow. To determine if an association exists between abdominal regional oxygen saturation (A-rSO2) and mesenteric blood flow, we compared changes in A-rSO2 to changes in blood flow velocity in the superior mesenteric artery (SMA) before and after feedings in very-low birthweight infants., Study Design: A-rSO2 was continuously monitored midline below the umbilicus for 3 days in 18 stable 25 to 31 week bolus-fed infants (median BW 1203 g, median age 5 days). We compared change in SMA velocity from immediately before to 10 min and 60 to 120 min after feeding with change in A-rSO2 over the same time. Spearman's rank correlation was used to ascertain if a significant association existed., Result: Change in A-rSO2 was significantly associated with change in systolic, diastolic, and mean SMA velocity from fasting to 60 to 120 min after feeding (P=0.016, 0.021, 0.010) and from 10 min after a feed to 60 to 120 min after feeding (P=0.009, 0.035, 0.032)., Conclusion: In very preterm infants, A-rSO2 reflects blood flow in the SMA and can provide non-invasive continuous monitoring of intestinal perfusion. Further studies are indicated to determine the sensitivity of NIRS to detect early intestinal pathology in this population.

In the present study, we tested the hypothesis that chronic treatment with the direct rennin inhibitor aliskiren improves the remodelling of resistance arteries in dTGR (double-transgenic rats). dTGR (5 weeks) were treated with aliskiren (3 mg/kg of body mass per day) or ramipril (1 mg/kg of body mass per day) for 14 days and compared with age-matched vehicle-treated dTGR. BP (blood pressure) was similarly reduced in both aliskiren-treated and ramipril-treated rats compared with control dTGR (167±1 and 169±2 mmHg compared with 197±4 mmHg respectively; P<0.05). The M/L (media-to-lumen) ratio assessed on pressurized preparations was equally reduced in aliskiren-treated and ramipril-treated rats compared with controls (6.3±0.5 and 6.4±0.2% compared with 9.8±0.4% respectively; P<0.05). Endothelium-dependent and -independent relaxations were similar among the groups. L-NAME (N(G)-nitro-L-arginine methyl ester) significantly reduced acetylcholine-induced dilation in drug-treated dTGR. This effect was significantly more prominent in aliskiren-treated rats. eNOS (endothelial NO synthase) expression showed a 2-fold increase only in aliskiren-treated dTGR as compared with controls (P<0.01) and ramipril-treated dTGR (P<0.05). Plasma nitrite, as an index of NO production, was significantly increased in dTGR treated with either aliskiren or ramipril compared with controls. Only aliskiren induced a 2-fold increase in plasma nitrite, which was significantly greater than that induced by ramipril (P<0.05). gp91(phox) expression and ROS (reactive oxygen species) production in aorta were significantly and similarly reduced by both drugs. In conclusion, equieffective hypotensive doses of aliskiren or ramipril reduced the M/L ratio of mesenteric arteries and improved oxidative stress in dTGR. However, only aliskiren increased further NO production in the vasculature. Hence, in dTGR, direct renin inhibition induces favourable effects similar to that induced by ACE (angiotensin-converting enzyme) inhibition in improving vascular remodelling through different mechanisms.

Background: The feeding interval is an important factor in enteral feeding of premature infants. We investigated postprandial intestinal blood flow in stable very-low-birthweight infants fed at 2-h and 3-h intervals., Methods: We used pulsed wave Doppler ultrasound to measure blood flow velocity of the superior mesenteric artery (SMA) before feeding and at 15, 30, 45, and 60 min after feeding. Measurements were made on the day of starting enteral nutrition (1 or 2 days of age), and at 3 and 5 days of age. A total of 21 studies were performed in seven infants fed every 2 h, and 54 studies were performed in 18 infants fed every 3 h., Results: In infants fed every 2 h, SMA blood flow velocity increased from before feeding to 30 min after feeding and then decreased at 60 min after feeding. In infants fed every 3 h, SMA blood flow velocity increased after feeding, reaching a peak at 30 min. The correlation coefficients between the volume of milk per feed and the postprandial increase in time-averaged mean blood flow velocity were 0.398 (P = 0.074, n = 21) and 0.597 (P = 0.000, n = 54) in infants fed at 2-h and 3-h intervals, respectively., Conclusions: SMA blood flow velocity significantly increased after feeding in infants fed at 2-h and 3-h intervals. The volume of milk per feed might affect the postprandial increase in SMA blood flow velocity., (© 2013 The Authors. Pediatrics International © 2013 Japan Pediatric Society.)

We present this preliminary investigation into the safety and feasibility of endovascular therapy for morbid obesity in a swine model. A flow-limiting, balloon-expandable covered stent was placed in the superior mesenteric artery of three Yorkshire swine after femoral arterial cutdown. The pigs were monitored for between 15 and 51 days after the procedure and then killed, with weights obtained at 2-week increments. In the two pigs in which the stent was flow limiting, a reduced rate of weight gain (0.42 and 0.53 kg/day) was observed relative to the third pig (0.69 kg/day), associated with temporary food aversion and signs of mesenteric ischemia in one pig.

The 33 amino acid peptide hormone GLP-2 is produced by enteroendocrine L-cells, the density of which is highest in the ileum and the colon, in response to the presence of nutrients in the lumen. The biological effect of GLP-2 is mediated by activation of a G-protein-coupled 7-transmembrane receptor. GLP-2 receptors are expressed in the brainstem, lungs, stomach, small intestine and colon, but not in the heart. It has been shown in several animal studies that GLP-2 infusion increases intestinal blood flow and that this increase is confined to the small intestine. The aim of the three studies, on which the thesis is based, was to investigate basic physiological effects of GLP-2, in healthy volunteers and in SBS patients, with focus on the effects on mesenteric blood flow, blood flow at other vascular sites and effects on cardiac parameters. These parameters have been evaluated after both meal stimulation and GLP-2 administration. The studies showed the following results: Blood flow: In all three studies, blood flow changes in the SMA after GLP-2 administration were similar regarding changes over time and degree of change. Blood flow changes were similar to changes seen after a standard meal. Only RI changes were registered in all three studies, but the TAMV changes in study 2 and 3 had similar characteristics. Cardiovascular parameters: In all three studies no significant changes in blood pressure were registered in relation to GLP-2 administration. In study two and three, where cardiac parameters also were registered by impedance cardiography, increases in CO and SV were seen. Plasma GLP-2: There were, as expected, supraphysiological GLP-2 plasma levels after SC administration. All three studies have shown rapid changes in mesenteric blood flow after administration GLP-2. The changes have been the same both in regards to time to maximum changes (increase) and relatively close in regards to maximum extent of change. The changes in the SBS patients were less than in the healthy test subjects. The findings leave no doubt about that GLP-2 is a potent regulator of upper splanchnic blood flow. The study findings also support the notion that the observed increased mesenteric blood flow, isolated to the SMA, is secondary to the metabolic responses to GLP-2, and that these are likely due to a paracrine action by GLP-2 acting on GLP-2R bearing cells such as enteric neurons, probably expressing NO. In conclusion GLP-2 increases mesenteric blood flow in healthy subjects and in SBS patients, the increase is equivalent to a standard meal and dose dependent. The blood flow is not increased at other arterial vascular sites. GLP-2 does not acutely alter blood pressure, but increases, probably as compensation, pulse rate and cardiac output. GLP-2 induced vascular response in the superior mesenteric artery is related with the length of remaining intestine in SBS patients. The effect is therefore likely to reflect the metabolic activity in the tissue rather than direct effect on the vascular system.

Background: Arterial hypertension is a multifactorial chronic condition caused by either congenital or acquired factors., Objective: To evaluate the effects of Resistance Training (RT) on arterial pressure, and on vascular reactivity and morphology, of L-NAME-treated hypertensive rats., Methods: Male Wistar rats (200 - 250 g) were allocated into Sedentary Normotensive (SN), Sedentary Hypertensive (SH) and Trained Hypertensive (TH) groups. Hypertension was induced by adding L-NAME (40 mg/Kg) to the drinking water for four weeks. Arterial pressure was evaluated before and after RT. RT was performed using 50% of 1RM, 3 sets of 10 repetitions, 3 times per week for four weeks. Vascular reactivity was measured in rat mesenteric artery rings by concentration-response curves to sodium nitroprusside (SNP); phenylephrine (PHE) was also used for histological and stereological analysis., Results: Resistance training inhibited the increase in mean and diastolic arterial pressures. Significant reduction was observed in Rmax (maximal response) and pD2 (potency) of PHE between SH and TH groups. Arteries demonstrated normal intima, media and adventitia layers in all groups. Stereological analysis demonstrated no significant difference in luminal, tunica media, and total areas of arteries in the SH and TH groups when compared to the SN group. Wall-to-lumen ratio of SH arteries was significantly different compared to SN arteries (p<0.05) but there was no difference when compared to TH arteries., Conclusions: RT was able to prevent an increase in blood pressure under the conditions in this study. This appears to involve a vasoconstrictor regulation mechanism and maintenance of luminal diameter in L-NAME induced hypertensive rats.

In the present study, we aimed to examine the effect of blockade of L-type Ca(2+) channels (LTCC) and in addition the removal of extracellular Ca(2+), on EFS-induced relaxations in rings of rat mesenteric artery. EFS applied to the tissues precontracted with phenylephrine caused relaxations which were markedly inhibited by nifedipine (10(-7)M) and tetraethylammonium (TEA) (1mM). Addition of LTCC opener BAY K 8644 (10(-7)M) failed to enhance the relaxations. Upon removal of Ca(2+), EFS with the same stimulation parameters produced frequency-dependent transient contractions. Tetrodotoxin (10(-6)M), capsaicin (10(-5)M) and removal of endothelium did not alter these contractions suggesting that they were not neural in origin and endothelium-derived contracting factors were unlikely to be involved. However, they were increased by nearly 40% in response to BAY K 8644 (10(-7)M) and were inhibited by nifedipine (10(-7)M), indicating that activation of the LTCCs was essential. Inositol triphosphate (InsP3) receptor antagonist 2-APB (10(-4)M) significantly reduced, and high concentration of caffeine (20mM) almost totally suppressed the contractions. These results suggest that in the absence of extracellular Ca(2+) EFS through membrane depolarization, evokes the opening of the LTCCs which subsequently leads to the release of Ca(2+) from internal stores via InsP3 receptors, a phenomenon known as Ca(2+) channel-induced Ca(2+) release (CCICR), to trigger vasoconstriction. That activation of LTCCs causes arterial relaxation or contraction depending on the Ca(2+) status apparently exemplifies how the same messenger fulfils opposing physiological functions in a given cell., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

The present study investigated the mechanisms underlying the vasorelaxant effects of the essential oil of Aniba canelilla (EOAC) and its main constituent 1-nitro-2-phenylethane (NP) in isolated superior mesenteric artery from spontaneously hypertensive rats (SHRs). At 0.1-1000 μg/mL, EOAC and NP relaxed SMA preparations pre-contracted with 75 mMKCl with IC(50) (geometric mean [95% confidence interval]) values of 294.19 [158.20-94.64] and 501.27 [378.60-624.00] μg/mL, respectively); or with phenylephrine (PHE) (IC(50)s=11.07 [6.40-15.68] and 7.91 [4.08-11.74) μg/mL, respectively). All these effects were reversible and remained unaltered by vascular endothelium removal. In preparations maintained under Ca(2+)-free conditions, EOAC and NP (both at 600 μg/mL) reduced the PHE-, but not the caffeine-induced contraction. In Ca(2+)-free and high K(+) (75 mM) medium, the contractions produced by CaCl(2) or BaCl(2) were reduced or even abolished by EOAC and NP at 100 and 600 μg/mL, respectively. EOAC and NP (both at 10-1000 μg/mL) also relaxed the contraction evoked by phorbol dibutyrate (IC(50)=52.66 [10.82-94.64] and 39.13 [31.55-46.72] μg/mL, respectively). It is concluded that NP has a myogenic endothelium-independent vasorelaxant effects and appears to be the active principle of the EOAC. Vasorelaxant effect induced by both EOAC and NP is preferential to receptor-activated pathways and it appears to occur intracellularly more than a superficial action restricted to the membrane environment such as a simple blocking activity on a given receptor or ion channel., (Copyright © 2013 Elsevier B.V. All rights reserved.)

Background: Hepatic artery variations are frequent clinical occurrences. The aim of this study was to investigate the characteristic course of variant hepatic arteries originating from the superior mesenteric artery for the purpose of providing instructions for abdominal tumor surgery., Methods: The course of variant hepatic arteries originating from the superior mesenteric artery was studied in 400 patients with liver cancer confirmed by digital subtraction angiography (DSA) and multi-slice spiral computed tomography angiography (MSCTA), and 86 patients with gastric cancer confirmed by preoperative MSCTA between June 2008 and June 2010 in the First Affiliated Hospital of Guangxi Medical University., Results: Hepatic artery variations originating from the superior mesenteric artery were noticed in 49 liver cancer patients and 14 gastric cancer patients (total 63 cases), with a variation rate of 12.96%, including two cases (3.17%) where the hepatic arteries ran along the anterior pancreas, and 61 cases (96.83%) where the hepatic arteries ran along the posterior pancreas., Conclusions: Hepatic artery variations originating from the superior mesenteric artery present as two types: the pre-pancreas type and the post-pancreas type with the latter predominating. This finding is of clinical significance in abdominal tumor surgeries where clearance of portal lymph nodes is needed.

Aim: Extracellular nucleotides activate cell-surface purinergic (P2) receptors, contribute to the local regulation of vascular tone and play important roles in pathophysiological states. However, little is known about the vasodilator effects of P2Y(1) -receptor activation in diabetic states. We hypothesized that in a model of established type 1 diabetes, long-term streptozotocin (STZ)-induced diabetic rats, the arterial relaxation elicited by a P2Y(1) -receptor agonist would be impaired., Methods: Relaxations to adenosine 5'-diphosphate sodium salt (ADP), 2-MeSADP (selective P2Y(1) -receptor agonist) and adenosine 5'-triphosphate disodium salt (ATP) were examined in superior mesenteric artery rings from long-term STZ-induced diabetic rats (at 50-57 weeks after STZ injection). ADP-stimulated nitric oxide (NO) production in the superior mesenteric artery was assessed by measuring the levels of NO metabolites. Mesenteric artery expressions of P2Y(1) receptor, and ADP-stimulated levels of phosphorylated endothelial NO synthase (eNOS) (at Ser(1177) and at Thr(495) ) and eNOS were detected by Western blotting., Results: Arteries from diabetic rats exhibited (vs. those from age-matched control rats): (i) reduced ADP-induced relaxation, which was partly or completely inhibited by endothelial denudation, by NOS inhibitor treatment and by a selective P2Y(1) -receptor antagonist, (ii) reduced 2-MeSADP-induced relaxation, (iii) reduced ADP-stimulated release of NO metabolites and (iv) impaired ADP-induced stimulation of eNOS activity (as evidenced by reduced the fold increase in eNOS phosphorylation at Ser(1177) with no difference in fold increase in eNOS phosphorylation at Thr(495) ). The protein expression of P2Y(1) receptor did not differ between diabetic and control arteries., Conclusions: These results suggest that P2Y(1) -receptor-mediated vasodilatation is impaired in superior mesenteric arteries from long-term type 1 diabetic rats. This impairment is because of reduced P2Y(1) -receptor-mediated NO signalling, rather than to reduced P2Y(1) -receptor expression., (© 2012 The Authors Acta Physiologica © 2012 Scandinavian Physiological Society.)

Background: Blood flow volume in the superior mesenteric artery (SMA) measured by pulsed Doppler has been used in adults to evaluate Crohn disease but has not been utilized in children and adolescents., Objective: To establish a cutoff point for normal SMA blood flow using pulsed Doppler US measurement in healthy children and adolescents., Materials and Methods: The study included healthy volunteers from an urban community, divided into two age groups, children (5-9 years) and adolescents (10-17 years). Anthropometric measurements included waist circumference and body surface area classified according to the z-score of body mass index. Heart rate, blood pressure, oxygen saturation and temperature were measured immediately before US evaluation., Results: The average age of the 60 participants was 12.2 years. Of these, 21 (35%) were ages 5-9 years and 39 (65%) were ages 10-17 years; 21 (35%) were boys. Findings of the two examiners coincided for 58 of the 60 (96.7%) participants. SMA blood flow was significantly lower in the children (mean ± SD = 556 ± 122 ml/min) than in adolescents (mean ± SD 775 ± 311 ml/min) (P < 0.001). SMA blood flow showed statistically significant positive associations with body surface area., Conclusion: We found that superior mesenteric artery blood flow is significantly lower in children than in adolescents and is associated with body surface area.