The relationship of foetal superior mesenteric artery blood flow and the time to first meconium passage in newborns with late-onset foetal growth restriction.

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 StatementWhat 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.

Yogic agnisara increases blood flow in the superior mesenteric artery.

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.

Trimethylamine-N-oxide (TMAO) Selectively Disrupts Endothelium-Dependent Hyperpolarization-Type Relaxations in a Time-Dependent Manner in Rat Superior Mesenteric Artery.

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.

Acrolein but not its metabolite, 3-Hydroxypropylmercapturic acid (3HPMA), activates vascular transient receptor potential Ankyrin-1 (TRPA1): Physiological to toxicological implications.

Acrolein, an electrophilic α,ß-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 EC50 0.8 ± 0.2 µM; aorta EC50 > 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).

Doppler ultrasound assessment of splanchnic perfusion and heart rate for the detection of necrotizing enterocolitis.

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.

Effects of Proximal and Distal Enteral Glucose Infusion on Cardiovascular Response in Health and Type 2 Diabetes.

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.

Pharmacological properties of ß-adrenoceptors mediating rat superior mesenteric artery relaxation and the effects of chemical sympathetic denervation.

AIMS: ß-Adrenoceptors (ß-ADRs) mediating the relaxation of rat superior mesenteric arteries (SMAs) were pharmacologically identified, and the effects of chemical sympathetic denervation on ß-ADR-mediated relaxation were examined. MAIN METHODS: The tension changes of endothelium-denuded SMAs were isometrically recorded and the mRNA of endothelium-denuded SMA ß-ADR was detected using RT-PCR. KEY FINDINGS: In endothelium-denuded SMAs contracted with ≥10-7 M phenylephrine (an α1-ADR agonist), isoprenaline (a ß-ADR agonist)-induced relaxation was competitively inhibited by 3 × 10-9-10-8 M propranolol (a ß1,2-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 ß2-ADR antagonist), it was competitively inhibited by atenolol (10-7-3 × 10-7 M; a ß1-ADR antagonist) in the presence of ICI-118,551. In the presence of 10-7 M propranolol, isoprenaline- and CGP-12177A (a ß3-ADR partial agonist)-induced relaxation was competitively inhibited by high concentrations of bupranolol (a ß1,2,3-ADR antagonist), with pA2 values of 6.49 and 5.76, respectively. We detected the mRNA of ß1- and ß3-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 ß1- and ß3-ADRs. ß-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 ß3-ADRs with different pharmacological properties.

Direct Impairment of the Endothelial Function by Acute Indoxyl Sulfate through Declined Nitric Oxide and Not Endothelium-Derived Hyperpolarizing Factor or Vasodilator Prostaglandins in the Rat Superior Mesenteric Artery.

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 (SKCa)- and intermediate (IKCa)-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.

Arterial blood supply to the pancreas from accessary middle colic artery.

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.

Superior mesenteric and renal flow patterns during intra-aortic counterpulsation.

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.

Effect of ivabradine, a funny current inhibitor, on portal hypertensive rats.

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.

Effect of caffeine on superior mesenteric artery blood flow velocities in preterm neonates.

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.

Influence of breakfast on hemodynamics after lunch - a sonographic evaluation of mesenteric and cervical blood flows.

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.

Royal jelly increases peripheral circulation by inducing vasorelaxation through nitric oxide production under healthy conditions.

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.

The optimal intestinal segment length for experimental size-mismatched intestinal transplantation: Defining the maximum length with the lowest blood flow needs in a porcine model.

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.

The effects of enteral feeding improvement massage on premature infants: A randomised controlled trial.

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 (Vmax ) and lower RI (resistant index). (iii) The experimental group of the feeding-intolerant subgroup had a higher superior mesentery artery Vmax and Vmin . (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.

The early postnatal blood flow characteristics in the superior mesenteric and coeliac arteries in late preterm neonates.

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 (EDVSMA) at 24 h and PSVTC 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 EDVSMA. Mean PIAMS 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.

Impaired endothelium-derived hyperpolarization-type relaxation in superior mesenteric arteries isolated from female Otsuka Long-Evans Tokushima Fatty rats.

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 NG-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.

Is visceral flow during intra-aortic balloon pumping size or volume dependent?

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 (t0), at 2-hour ischemia (t1) and every hour thereafter until 6 hours of reperfusion (from tR1 to tR6). RESULTS: SMA flows increased significantly at tR1 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.

Tunicamycin-Induced Alterations in the Vasorelaxant Response in Organ-Cultured Superior Mesenteric Arteries of Rats.

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.