Increase In Mesenteric Blood Flow Research Articles

Postprandial Increase in Mesenteric Blood Flow is Attenuated in Parkinson's Disease: A Dynamic PC-MRI Study.

Background:Gastrointestinal dysfunction and related clinical symptoms are common in Parkinson’s disease (PD), but the underlying mechanisms are still poorly understood.Objective:In this study, we investigated how PD affects the postprandial vascular response in the splanchnic circulation.Methods:23 patients with PD in the “ON-medication” state and 23 age- and sex-matched healthy control participants underwent serial phase-contrast magnetic resonance imaging (PC-MRI) to measure the postprandial blood flow response in the superior mesenteric artery (SMA). Participants ingested a standardized liquid test meal (∼400 kcal) and underwent four PC-MRI runs within the following hour. Each PC-MRI run consisted of six consecutive measurements of SMA blood flow.Results:In both groups, standardized food intake triggered an increase of blood flow in the SMA, but absolute and relative increases in blood flow were attenuated in patients compared to the control group (p < 0.001). While baseline blood flow in the SMA was comparable in both groups, the postprandial maximum blood flow was attenuated in patients (p = 0.03). The temporal dynamics of the postprandial blood flow did not differ between groups. Postprandial SMA blood flow increase in patients correlated neither with subjective reports of non-motor symptoms or upper gastrointestinal complaints, nor with levodopa equivalent daily dose or disease duration. Blood glucose measurements in between the PC-MRI runs showed a smaller postprandial increase in blood glucose in the patient group (p = 0.006).Conclusion:This study provides first-time evidence that patients with PD have an attenuated postprandial blood flow response in the SMA, indicating an impaired functional regulation of gastrointestinal perfusion in response to food intake in PD.

Nutrient stimulation of mesenteric blood flow - implications for older critically ill patients.

Nutrient ingestion induces a substantial increase in mesenteric blood flow. In older persons (aged ≥ 65 years), particularly those with chronic medical conditions, the cardiovascular compensatory response may be inadequate to maintain systemic blood pressure during mesenteric blood pooling, leading to postprandial hypotension. In older ambulatory persons, postprandial hypotension is an important pathophysiological condition associated with an increased propensity for syncope, falls, coronary vascular events, stroke and death. In older critically ill patients, the administration of enteral nutrition acutely increases mesenteric blood flow, but whether this pathophysiological response is protective, or precipitates mesenteric ischaemia, is unknown. There are an increasing number of older patients surviving admission to intensive care units, who are likely to be at increased risk of postprandial hypotension, both during, and after, their stay in hospital. In this review, we describe the prevalence, impact and mechanisms of postprandial hypotension in older people and provide an overview of the impact of postprandial hypotension on feeding prescriptions in older critically ill patients. Finally, we provide evidence that postprandial hypotension is likely to be an unrecognised problem in older survivors of critical illness and discuss potential options for management.

Systemic Cholecystokinin Differentially Affects Baro-activated GABAergic Neurons in Rat Caudal Ventrolateral Medulla

Cholecystokinin (CCK) is released after a meal to promote digestion and satiety. Circulating CCK inhibits splanchnic sympathetic nerve activity (sSNA), which may contribute to postprandial increases in mesenteric blood flow. The CCK-induced sympathoinhibition occurs by activation of vagal afferent nerves and inhibition of a subset of presympathetic rostral ventrolateral medullary (RVLM) neurons. The present study sought to determine whether the caudal ventrolateral medulla (CVLM) may also play a role in the CCK-induced changes in sSNA. Rats were anesthetized with chloralose, artificially ventilated, paralyzed, and prepared for recording arterial pressure (AP), heart rate (HR), sSNA, and activity of individual CVLM neurons. Injection of CCK-8 (8-10 microg/kg, iv) decreased sSNA, AP, and HR. Most baro-activated CVLM neurons were excited by CCK (n = 25, 3.4-fold increase), whereas other baro-activated CVLM neurons were not affected (n = 7) or were inhibited (n = 3). A subset of baro-activated CVLM neurons that were activated (n = 8) or unaffected (n = 2) was confirmed to be GABAergic by the presence of GAD67 mRNA. Bilateral inhibition of the CVLM by microinjections of muscimol reversed the decreases in sSNA and AP to a prominent sympathoactivation and increase in AP (n = 18). These data suggest that systemic injection of CCK leads to the activation of most baro-activated GABAergic CVLM neurons and that the CVLM is essential for the production of CCK-induced inhibition of sSNA. The differential responses of baro-activated GABAergic CVLM neurons to CCK may contribute to the diverse responses of presympathetic RVLM neurons and sympathetic outflows observed with systemic CCK.

Understanding the splenic contribution to portal flow: The role of splenic artery ligation as inflow modification in living donor liver transplantation

Understanding the splenic contribution to portal flow: The role of splenic artery ligation as inflow modification in living donor liver transplantation

Systemic and splanchnic haemodynamic effects of sildenafil in an in vivo animal model of cirrhosis support for a risk in cirrhotic patients.

Sildenafil is a selective inhibitor of the cGMP-specific phosphodiesterase type V (PDE-V) in the corpus cavernosum. PDE-V is also present in the mesenteric artery. Cirrhosis is complicated by a splanchnic vasodilation attributed to a local overproduction of nitric oxide (NO). As sildenafil potentiates the effects of NO, it may further decrease mesenteric vascular tone and increase portal venous blood flow. The aim is to evaluate the effects of sildenafil on the systemic and splanchnic haemodynamics in an experimental model of cirrhosis. Secondary biliary cirrhosis was induced in male Wistar rats by common bile duct ligation (CBDL, n=8); control rats were sham-operated (sham, n=7). The mean arterial pressure (MAP), portal venous pressure (PVP) and arterial mesenteric blood flow (MBF) were measured after intramesenteric (0.01-10 mg/kg) and after intravenous (i.v.) (0.01-10 mg/kg) administration of sildenafil. Baseline PVP was significantly higher in CBDL than in sham rats, whereas baseline MAP tended to be lower and MBF tended to be higher in CBDL compared with sham rats. Both intramesenteric and i.v. injection of sildenafil significantly decreased MAP and increased MBF and PVP in a dose-dependent way. The decrease in MAP was significantly less important in CBDL than in sham rats. The increase in MBF was importantly lower in CBDL than in sham rats. PVP tended to increase more significantly in sham rats than in CBDL. Sildenafil increases MBF and PVP and induces systemic hypotension. The effects are less pronounced in cirrhosis, suggesting vascular hyporesponsiveness to sildenafil. Although the rise in PVP in cirrhotic animals is smaller than in controls, it may present a risk for haemorrhagic complications. Further studies are necessary before prescribing sildenafil to patients with cirrhosis.

Feeding the Hypotensive Patient: Does Enteral Feeding Precipitate or Protect Against Ischemic Bowel?

Although the enteral route of enteral feeding is the preferred method of nutrition support for critically ill patients, this important therapeutic strategy is not without risk. In human subjects, the digestion and absorption of nutrients induce typical hemodynamic changes, consisting of an increase in mesenteric blood flow at the expense of reduced systemic blood pressure. On rare occasion when providing aggressive enteral nutrition to critically ill patients, common symptoms of gastrointestinal intolerance may progress to a syndrome of abdominal distention, hypotension, and shock, with the development of small bowel ischemia or necrosis. Although the incidence of small bowel ischemia secondary to enteral feeding is low, the overall clinical outcome is still poor and carries a high mortality rate. Enteral feeding is well tolerated and is probably beneficial in most critically ill patients before and after a period of hypotension. Although enteral nutrition may be used with caution during the period of hypotension, evidence of poor gastrointestinal function (increased nasogastric tube output, unexplained abdominal pain, and abdominal distention), or development of dilated loops of bowel or intramural gas (pneumatosis intestinalis) on radiographic studies should be interpreted as potential indicators of gut ischemia. With progress in our understanding of the pathophysiology, diagnosis, and prevention of ischemic injury to the intestinal mucosa, the strategy of aggressive enteral feeding for critically ill patients may result in a reduction in this major complication and enhanced functional recovery from severe illness.

The effect of 17beta-oestradiol on regional blood flow in anaesthetized pigs.

1. The present study was designed to investigate the effects of 17beta-oestradiol on the mesenteric, renal, iliac and coronary circulations and to determine the mechanisms involved. 2. In pigs anaesthetized with sodium pentobarbitone, changes in blood flow in the superior mesenteric, left renal, left external iliac and left circumflex coronary arteries caused by intravenous infusion of 17beta-oestradiol at constant heart rate and arterial pressure were assessed using electromagnetic flowmeters. 3. In eight pigs, infusion of 2 microg h-1 of the hormone caused an increase in renal, iliac and coronary blood flow without affecting mesenteric blood flow, left ventricular dP/dtmax (rate of change of left ventricular systolic pressure) and filling pressures of the heart. In four pigs, these vasodilator effects were enhanced by graded increases in the dose of the hormone between 1, 2 and 3 microg h-1; the highest dose also caused an increase in mesenteric blood flow. 4. In five pigs, blockade of muscarinic cholinoceptors and adrenoceptors with the intravenous administration of atropine, propranolol and phentolamine did not affect the vasodilator responses caused by infusion of 2 microg h-1 of 17beta-oestradiol. 5. The increases in renal, iliac and coronary blood flow caused by infusion of 2 microg h-1 of 17beta-oestradiol were prevented, respectively, by the injection of Nomega-nitro-L-arginine methyl ester (L-NAME) into the renal artery (five pigs), the iliac artery (five pigs) or the coronary artery (five pigs). In five pigs, all responses were prevented by injection of L-NAME into all three arteries. In two pigs, injection of L-NAME into the mesenteric, renal, iliac and coronary arteries abolished the vasodilator responses to the infusion of 3 microg h-1 of 17beta-oestradiol. 6. The present study shows that intravenous infusion of 2 microg h-1 of 17beta-oestradiol primarily dilated renal, iliac and coronary circulations and that a higher dose of the hormone also caused vasodilatation in the mesenteric vascular bed. The mechanism of these responses was shown to be nitric oxide dependent.

Fat and Mesenteric Blood Flow

Background: The introduction of fat to the duodenum leads to an increase in mesenteric blood flow. The exact mechanism, however, is unknown. In this study we investigate the influence of the terminal carboxy group of the oleic acid molecule on superior mesenteric artery blood flow. Methods: In six healthy male volunteers duplex ultrasound was used to evaluate the effects of duodenal perfusion of 48 mmol oleic acid and 48 mmol oleyl alcohol on superior mesenteric artery blood flow variables and diameter. Results: The blood flow variables time-average velocity and maximal diastolic velocity increased significantly, and the resistance index decreased significantly during perfusion with oleic acid, but during oleyl alcohol perfusion no changes were found. No significant changes in vessel diameter were observed at any time. Conclusion: The carboxy group of the oleic acid molecule has an important role in the duodenum in mediating the postprandial increase in superior mesenteric artery blood flow.

Vasoactivity and immunoreactivity of fish tachykinins in the vascular system of the spiny dogfish.

Tachykinin control of gut blood flow (measured by pulsed Doppler technique), dorsal aortic pressure, and heart rate were studied in unrestrained spiny dogfish Squalus acanthias injected with the elasmobranch tachykinins scyliorhinin I and II (SCY I and SCY II), the trout tachykinins substance P (SP), and neurokinin A (NKA). Effects on somatic vasculature were measured by in vitro perfusion of the isolated tail. SCY I and trout SP produced hypotension due to a general vasodilation. This caused a transient increase in mesenteric blood flow and a prolonged increase in celiac blood flow. SCY II caused an initial hypertension induced by a general vasoconstriction, followed eventually by an elevated flow in both gut arteries due to dilation of the vascular beds. Trout NKA evoked a short-lasting increase in celiac blood flow due to a decrease in vascular resistance, a late decrease in mesenteric flow due to vasoconstriction, and no effect on the somatic vasculature. None of the peptides affected heart rate. The study demonstrates a significant vasoactive function of fish tachykinins in the vascular system of an elasmobranch species and, in addition, the occurrence of tachykinin receptor subtypes. Immunohistochemistry revealed a NKA/SCY II-like peptide in nerve fibers innervating many vessels, including the celiac and the mesenteric arteries, the gastrointestinal canal, and the heart.

Inhibitory Effects of Emedastine Difumarate on Histamine Release

The present study was performed to clarify the mechanism of vasodilation of KRN2391 in canine mesenteric artery compared with those of nicorandil and cromakalim. We used the responses of isolated cranial mesenteric artery in vitro and changes in mesenteric blood flow in vivo as indicators reflecting the responses of a conductive artery and resistive arterioles, respectively. In isolated cranial mesenteric artery, KRN2391 (10(-8)-10(-5) M), nicorandil (10(-7)-10(-4) M) and cromakalim (10(-7)-10(-5) M) relaxed contractions caused by 25 mM KCl in a concentration-dependent manner. The concentration-relaxation curve for KRN2391 was shifted to the right by either methylene blue (10(-5) M) or glibenclamide (10(-6) M), but the inhibitory effect of methylene blue was more potent than that of glibenclamide. The concentration-relaxation curve for nicorandil was shifted to the right by methylene blue, but not by glibenclamide. In addition, the curve for cromakalim was shifted to the right by glibenclamide, but not by methylene blue. In in vivo experiments, the injections of KRN2391 (0.3-3 micrograms/kg), nicorandil (10-100 micrograms/kg) or cromakalim (1-10 micrograms/kg) into the mesenteric artery increased mesenteric blood flow in a dose-dependent manner. Glibenclamide (5 mg/kg, i.v.) attenuated the increase in mesenteric blood flow caused by KRN2391, nicorandil and cromakalim, but had no effect on that caused by nifedipine (1 microgram/kg). The ED20 value increased about 4.7-fold for KRN2391, 3.7-fold for nicorandil and 11.5-fold for cromakalim after administration of glibenclamide, as estimated from the % change to the absolute increase in mesenteric blood flow induced by nifedipine (1 microgram/kg).(ABSTRACT TRUNCATED AT 250 WORDS)

Involvement of beta 2-adrenoceptors in the regional haemodynamic responses to bradykinin in conscious rats.

1. Bradykinin can release neuronal calcitonin gene-related peptide (CGRP) and adrenal medullary catecholamines, both of which could contribute to its cardiovascular effects in vivo. Therefore, in the main experiment, regional haemodynamic responses to bolus injections of bradykinin (3 nmol kg-1, i.v.) were assessed in the same chronically-instrumented, conscious, Long Evans rats in the absence and in the presence of human alpha-CGRP [8-37] or ICI 118551, antagonists of CGRP1-receptors and beta 2-adrenoceptors, respectively. The selected doses of these antagonists caused specific inhibition of responses mediated by exogenous human alpha-CGRP and beta 2-adrenoceptor agonists, respectively. 2. Bradykinin administered alone as an i.v. bolus had a slight pressor effect accompanied by a marked tachycardia. There were early (at about 30 s) increases in flow and conductance in the mesenteric vascular bed, and delayed (at about 90 s), but qualitatively similar, changes in the hindquarters vascular bed. There were only slight increases in flow and conductance in the renal vascular bed. 3. Human alpha-CGRP [8-37] had no statistically significant effects on the responses to bolus doses of bradykinin. However, in the presence of ICI 118551, the pressor effect of bradykinin was significantly enhanced while its tachycardic effect was significantly suppressed. The hindquarters vasodilator effect of bradykinin was converted to a vasoconstriction and there was a slight renal vasoconstriction, but the mesenteric vasodilator effect of bradykinin was unchanged by ICI 118551. 4. In subsidiary experiments, in other animals, it was found that infusion of bradykinin (36 nmol kg-1 min-1) elicited a pattern of haemodynamic responses similar to that seen with bolus injections and, as in the latter case, the hindquarters hyperaemic vasodilation was inhibited by ICI 118551. In the presence of mecamylamine (at a dose sufficient to block reflex heart rate responses to rises or falls in arterial blood pressure) bolus injection or infusion of bradykinin still elicited increases in renal, mesenteric and hindquarters blood flow. However, in additional experiments in adrenal demedullated rats (n = 4) the hindquarters hyperaemic effect of bradykinin was absent, although the mesenteric hyperaemic effect remained. 5. The results indicate that the increase in hindquarters blood flow following administration of bradykinin in vivo is largely due to activation of beta 2-adrenoceptors by catecholamines released subsequent to direct stimulation of the adrenal medulla by the peptide. However, the bradykinin-induced increase in mesenteric blood flow does not depend on this mechanism.

Selective dopamine DA1 stimulation with fenoldopam in cirrhotic patients with ascites: A systemic, splanchnic and renal hemodynamic study

We studied the effects of fenoldopam, a selective dopamine DA1 agonist on systemic and splanchnic hemodynamics, renal blood flow and sodium excretion in 12 patients with alcoholic cirrhosis and ascites. Hepatic, azygos and renal veins were catheterized before and after intravenous administration of fenoldopam, 0.05 μg/kg/min for 1 hr and increased to 0.1 μg/kg/min for another hour. Mean arterial pressure progressively decreased (from 83 ± 7 to a minimum of 77 ± 8 mm Hg 100 min after starting the infusion) but returned to baseline level at 120 min. Plasma norepinephrine and renin activity increased (respectively from 567 ± 297 to 919 ± 375 pg/ml, p < 0.05, and from 17 ± 14 to 23 ± 15 ng/ml/hr, p < 0.05). Renal blood flow, urine output or sodium excretion did not change. Sodium output decreased at 1 hr from 6.9 μmol/min to 4.0 μmol/min, p < 0.05. Both hepatic venous pressure gradient and azygos blood flow significantly increased by 21%. We conclude that the acute administration of fenoldopam did not improve renal hemodynamics or function in patients with cirrhosis and ascites. In addition, dopamine DA1 agonism caused further increases in norepinephrine concentration and plasma renin activity. Portal pressure also increased, probably because of an increase in mesenteric blood flow. These results question the renal benefit and raise concern about the use of dopamine agonists in patients with cirrhosis and ascites. (HEPATOLOGY 1991;13:111–116).

Selective dopamine DA1 stimulation with fenoldopam in cirrhotic patients with ascites: A systemic, splanchnic and renal hemodynamic study

We studied the effects of fenoldopam, a selective dopamine DA1 agonist on systemic and splanchnic hemodynamics, renal blood flow and sodium excretion in 12 patients with alcoholic cirrhosis and ascites. Hepatic, azygos and renal veins were catheterized before and after intravenous administration of fenoldopam, 0.05 micrograms/kg/min for 1 hr and increased to 0.1 micrograms/kg/min for another hour. Mean arterial pressure progressively decreased (from 83 +/- 7 to a minimum of 77 +/- 8 mm Hg 100 min after starting the infusion) but returned to baseline level at 120 min. Plasma norepinephrine and renin activity increased (respectively from 567 +/- 297 to 919 +/- 375 pg/ml, p less than 0.05, and from 17 +/- 14 to 23 +/- 15 ng/ml/hr, p less than 0.05). Renal blood flow, urine output or sodium excretion did not change. Sodium output decreased at 1 hr from 6.9 mumol/min to 4.0 mumol/min, p less than 0.05. Both hepatic venous pressure gradient and azygos blood flow significantly increased by 21%. We conclude that the acute administration of fenoldopam did not improve renal hemodynamics or function in patients with cirrhosis and ascites. In addition, dopamine DA1 agonism caused further increases in norepinephrine concentration and plasma renin activity. Portal pressure also increased, probably because of an increase in mesenteric blood flow. These results question the renal benefit and raise concern about the use of dopamine agonists in patients with cirrhosis and ascites.

Anatomical Localization of the Binding and Functional Characterization of Responses to Dopexamine Hydrochloride in the Rat Mesenteric Vasculature

Dopamine receptors of the DA1 subtype have been identified in mesenteric blood vessels, stimulation of which leads to vasodilation. In this study, we have determined the anatomical localization of dopexamine-hydrochloride-binding sites and carried out functional characterization of responses to this DA1-receptor and beta 2-adrenoceptor agonist in rat mesenteric vasculature. Autoradiographic studies showed the presence of [3H]-dopexamine-binding sites in all the different layers of the mesenteric artery. The DA1 receptor antagonist, SCH 23390 (IC50 = 4.9 mumol/l), and the beta-adrenoceptor antagonist, propranolol (IC50 = 6.0 mumol/l), inhibited the binding of dopexamine. The inhibitory effect of these compounds on dopexamine binding was selective for different regions of the mesenteric artery. Also, dopexamine produced concentration-related increases in cAMP formation in membrane particles from superior mesenteric artery and its main branches. The presence of both SCH 23390 and propranolol was required to completely abolish dopexamine-induced increases in cAMP formation. In functional studies, dopexamine (1 and 3 micrograms/kg/min) produced dose-related increases in mesenteric blood flow (23 and 38%, respectively) which were accompanied by concomitant decreases in the calculated mesenteric vascular resistance. As seen with increases in cAMP, the vascular responses to dopexamine could be completely abolished only by prior treatment with both SCH 23390 and propranolol. These results suggest that in mesenteric vasculature of rat dopexamine binds primarily to DA1 receptors and beta 2-adrenoceptors. The activation of these receptors by dopexamine leads to vasodilation which is mediated by an increase in the intracellular levels of cAMP.

Mechanism of “substance P”: On mesenteric blood flow; Interactions with opioid peptides

The effects of close intra arterial injection of substance P (SP) and the interaction of SP with opioid peptides, have been studied on mesenteric blood flow in the anaesthetized dog. Injection of SP into the superior mesenteric artery caused a dose dependent increase in mesenteric blood flow. This effect was enhanced by pretreatment with the alpha 2 adrenergic antagonist yohimbine. The action of SP was significantly reduced by pretreatment with muscarinic and nicotinic cholinergic, dopamine and histamine (H 1) receptor antagonists. Beta adrenergic, histamine (H 2) and opiate receptor antagonists did not influence the action of SP. Pretreatment with tetrodotoxin partially inhibited the effect of SP, indicating that as well as a neurogenic action, it has a direct action on the vascular smooth muscle. The effect of SP was enhanced by D-Met 2-NleS 5-enkephalinamide, a delta opiate receptor agonist. The actions of D-Met 2-NleS 5-enkephalinamide were abolished by pretreatment with hexamethonium, partially abolished by naloxone but were unaffected by atropine. The mu opiate receptor agonist, D-Met 2-Pro 5-enkephalinamide, inhibited the effects of SP.

The phenomenon and cause of the dose-dependent oral absorption of chlorothiazide in rats: Extrapolation to human data based on the body surface area concept

The reported incomplete and dose-dependent absorption of chlorothiazide in humans was demonstrated in six rats after five oral solutions at doses of 0.93, 2.55, 9.23, 25.6, and 70.2 mg/kg. Mean 48-hr urinary recoveries of intact drug were 57.3, 50.4, 36.7, 22.8, and 15.3%, respectively. A similar degree of dose dependency in absorption was found in rat, dog, and human when the doses were related to unit body surface area (BSA) but not on unit body weight, indicating similar interspecies absorptive capacity in terms of unit BSA. This finding may be partly rationalized by marked similarities in the reported solution transit time (2-3 hr) in the small intestine as well as in the calculated gross surface area of the small intestine per unit BSA (0.163 for rat and 0.132 for human). Contrary to the previous postulation of a specific absorption site, the drug was absorbed from different regions of the GI tract with apparent 1-hr absorption rates, studied by the in situ closed-loop method, in the following rank order: jejunum (34.6%) greater than duodenum (32.7%) greater than large intestine (20.1%) greater than ileum (18.0%) greater than stomach (12.4%). Different from the commonly assumed first-order absorption process, the intestinal loop absorption was concentration-dependent, suggesting a saturable mechanism. For example, the absorption rate at 0.008 mg/mL was higher than that at 0.2 mg/mL in ileal loops (61%, p less than 0.01) and jejunal loops (22%, p less than 0.1). In addition, the absorption rates at pH 6 and 7.4 were statistically identical, indicating a lack of ionization effect that is important in the passive absorption process. The solubility-limited absorption could probably be ruled out at doses below 2.55 mg/kg for rat and 125 mg for human in view of higher aqueous solubilities at 37 degrees C (e.g., 1.3 mg/mL at pH 7) found in the present study. Contrary to the previous hypothesis of low membrane permeability as a limiting factor for absorption, the "intrinsic" partition coefficient in 1-octanol/aqueous buffer was moderate, 0.6. Furthermore, the absorption in ileal and jejunal loops was enhanced by an apparent increase in mesenteric blood flow by caffeine. The existence of prolonged oral absorption in rats and humans is discussed.

Evidence for a role of capsaicin-sensitive mucosal afferent nerves in the regulation of mesenteric blood flow in the dog

Capsaicin injected into the lumen of the small intestine produced marked changes in mesenteric blood flow in anesthetized dogs. In the majority of cases capsaicin evoked a significant increase in mesenteric blood flow, the time-course of which indicated it was of a reflex nature. The response to capsaicin was completely abolished by a previous intraluminal application of the local anesthetic lidocaine, and was inhibited by an intraarterial injection of somatostatin. The present findings suggest that the effects of capsaicin may be related to a release of vasoactive peptides from afferent nerves associated with the vascular system of the gastrointestinal tract. It is concluded that capsaicin-sensitive mucosal afferent nerves, possibly provided with an axon reflex arrangement, may play a role in the regulation of local intestinal blood flow.

Hemodynamic effects of a new histamine H 2 receptor agonist (impromidine) and antagonist (ranitidine)

Summary The current study was designed to evaluate a) the effects of a relatively new histamine H2 receptor antagonist, ranitidine, on H2 mediated increases in canine renal and mesenteric blood flows and b) the effects of a relatively new H2 agonist, impromidine, on canine mesenteric hemodynamics. Ranitidine was nearly 10 times as effective as cimetidine (a widely prescribed H2 antagonist) in inhibiting dimaprit (an H2 agonist) induced increases in renal and mesenteric blood flows. Studies with impromidine revealed that this H2 agonist is about 100 times more potent than dimaprit in producing equivalent increases in mesenteric blood flow.

Effects of methionine-enkephalin on intestinal circulation and oxygen consumption.

AbstractThe effects of intra-arterial administration of Met-enkephalin upon intestinal blood flow, oxygen consumption, intestinal motor activity, and distribution of blood flow to the compartments of the gut wall were measured in anesthetized dogs before and after blockade of opiate receptors with naloxone. Blood flow to a segment of distal ileum was measured with an electromagnetic blood flow meter and intestinal oxygen extraction was measured spectrophotometrically. Oxygen uptake was calculated as the product of oxygen extraction and total blood flow. Changes in blood flow distribution were estimated from the distribution of radiolabeled microspheres. Motor activity was monitored from changes in intraluminal pressure. In dogs prior to blockade of opiate receptors, Met-enkephalin induced a dose-related increase in mesenteric blood flow, oxygen extraction and consumption, and intestinal motor activity. A significant increase in blood flow to the muscularis was also observed. The intestinal vasodilator, me...

Effects of a rapid injection into the canine superior mesenteric artery of diatrizoate meglumine and diatrizoate sodium (Renografin-76).

In an effort to evaluate the "spillover method" of measuring blood flow during angiography, we explored the effects of rapid injection of diatrizoate meglumine and diatrizoate sodium (Renografin-76) at rates no greater than resting blood flow in the superior mesenteric artery of anesthetized dogs. An increase in mesenteric blood flow and a decrease in mesenteric arterial pressure occurred many seconds after cessation of the injection. The dilation effected by the contrast agent was less marked at elevated blood flow values than at resting flows. The pattern of response to diatrizoate meglumine and diatrizoate sodium resembled that observed with vasodilator drugs. Our findings also suggest that the initial vascular response to a pulsation of the diatrizoate medium is vasodilation.