Biomedical subjects

J N Benoit

Publications and source records attributed to J N Benoit.

At least 55 records · Page 3Linked to original sources

PubMed1986

Splanchnic hemodynamics in chronic portal hypertension.

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Animals↗

PubMed1986

Chronic portal hypertension: effects on gastrointestinal blood flow distribution.

The intramural distribution of blood flow in the gastrointestinal tract was measured in shamoperated control and portal vein-stenosed rats. Total organ blood flow, measured via the radioactive microsphere technique, was elevated in the esophagus (66%), stomach (102%), duodenum (42%), jejunum (52%), ileum (54%), and colon (79%) of portal-hypertensive rats. Histological evaluation of carbonized nonradioactive 15-microns microspheres allowed for fractionation of blood flow within the wall (mucosa, submucosa, and muscularis externa) of each organ. The microsphere distribution pattern indicates that intramural blood flow distribution in all organs was not dramatically affected by chronic portal hypertension. These findings further define the characteristics of the factors responsible for the gastrointestinal hyperemia produced by chronic portal hypertension.

Animals↗

PubMed1986

Role of glucagon in splanchnic hyperemia of chronic portal hypertension.

The role of glucagon as a blood-borne mediator of the hyperdynamic circulation associated with chronic portal venous hypertension was assessed in the rat portal vein stenosis model. Selective removal of pancreatic glucagon from the circulation was achieved by intravenous infusion of a highly specific glucagon antiserum. Blood flow to splanchnic organs, kidneys, and testicles was measured with radioactive microspheres, and the reference-sample method. Glucagon antiserum had no effect on blood flow in the gastrointestinal tract of sham-operated (control) rats. However, the antiserum produced a significant reduction in hepatic arterial blood flow in the control rats, suggesting that glucagon contributes significantly to the basal tone of hepatic arterioles. In portal hypertensive rats glucagon antiserum significantly reduced blood flow to the stomach (22%), duodenum (25%), jejunum (24%), ileum (26%), cecum (27%), and colon (26%). Portal venous blood flow was reduced by approximately 30%. The results of this study support the hypothesis that glucagon mediates a portion of the splanchnic hyperemia associated with chronic portal hypertension.

Animals↗

PubMed1986

Role of free radicals in ischemia-reperfusion injury to the liver.

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Alanine Transaminase↗

PubMed1985

Reduced vascular sensitivity to norepinephrine in portal-hypertensive rats.

The development of portal hypertension following chronic portal vein stenosis is accompanied by a significant increase in intestinal blood flow. The present study was designed to determine whether intestinal vascular sensitivity to norepinephrine (NE) is also affected by chronic portal vein stenosis. Using a blood-perfused, in situ rat small intestine preparation, we found that, when compared with control animals, a significantly greater molar concentration of NE was required to achieve the same proportional increase in intestinal vascular resistance in portal-hypertensive animals. The mean ED50 value (+/-SE) for the portal-hypertensive group (704.3 +/- 186.1 nM) was significantly greater (P less than 0.05) than the mean ED50 value for the control group (271.4 + 48.1 nM). This finding implies that sympathetic maintenance of intestinal vascular tone may be impaired following chronic portal vein stenosis, possibly accounting for part of the intestinal hyperemia associated with portal hypertension.

Animals↗

PubMed1985

Humoral factors may mediate increased rat hindquarter blood flow in portal hypertension.

Chronic portal hypertension is associated with systemic hypotension and reduced peripheral vascular resistance. Although it is well established that splanchnic and renal vascular resistances are reduced, the contribution of possible alterations in skeletal muscle hemodynamics in portal hypertension is unknown. The present study was designed to determine if skeletal muscle vascular resistance was reduced and blood flow increased in portal hypertensive rats. In portal hypertensive animals, hind-quarter blood flow was significantly increased while vascular resistance was significantly reduced. The fall in resistance in the portal hypertensive animals was associated with an increase in the capillary filtration coefficient, suggesting that an increase in functional exchange vessel surface area occurred. Cross perfusion of control hindquarters with portal hypertensive blood resulted in a 38% reduction in hindquarter vascular resistance. Raising the plasma glucagon concentration to levels reported in portal hypertensive animals resulted in no change in blood flow or vascular resistance in control hindquarters. Skeletal muscle vascular sensitivity to norepinephrine was assessed by constructing dose-response curves in control and portal hypertensive animals. Mean ED50 values were not different. The results of these studies indicate that skeletal muscle vascular resistance is reduced in portal hypertension and humoral factors, but not glucagon, are primarily responsible for the skeletal muscle hyperemia associated with portal hypertension.

Animals↗

PubMed1985

"Forward" and "backward" flow mechanisms of portal hypertension. Relative contributions in the rat model of portal vein stenosis.

The contribution of "forward" and "backward" flow mechanisms to the increased portal pressure observed in the rat model of portal vein stenosis was evaluated using experimental and theoretical data. The experimental data indicate that portal venous inflow, portasystemic shunting, and portal venous pressure are increased after 10 days of portal vein stenosis when compared with sham-operated controls. Furthermore, portal vascular resistance was 40% higher in portal hypertensive animals than in control animals. The elevated portal vascular resistance in the rat with portal vein stenosis was attributed to the high resistance of the portal venous collaterals. Incorporation of the experimental data into a mathematical model that simulated the changes induced by chronic portal vein stenosis allowed for fractionation of the "forward" and "backward" flow components involved in the pathogenesis of portal hypertension. Model predictions indicate that the "forward" and "backward" flow mechanisms account for 40% and 60% of the increase in portal pressure, respectively.

Animals↗

PubMed1984

A rat model for studying the intestinal circulation.

A preparation is described that allows for whole-organ studies on the rat intestinal microcirculation. The preparation is an in situ autoperfused segment of small intestine. An arterial perfusion circuit is established between the carotid and superior mesenteric arteries and a venous circuit between the superior mesenteric and jugular veins. This model allows for measurements of superior mesenteric arterial and venous pressures, blood flow, arteriovenous oxygen difference, lymph flow, capillary pressure, capillary reflection coefficient, and the capillary filtration coefficient. Preliminary studies using this model indicate a resting blood flow of approximately 120 ml X min-1 X 100 g-1. Resting intestinal oxygen consumption is approximately two to three times the value reported for dogs and cats. Experiments were performed to assess the responses of the preparation to commonly employed physiological perturbations, including pressure-flow autoregulation, functional hyperemia, and response to venous pressure elevations. The observed responses are consistent with intrinsic control of resistance and exchange vessels. The model should prove useful for future studies regarding the physiology and pathology of intestinal hemodynamics, oxygenation, and capillary fluid exchange.

Animals↗

PubMed1984

Role of humoral factors in the intestinal hyperemia associated with chronic portal hypertension.

The role of neural, metabolic, physical, and humoral factors in the intestinal hyperemia associated with chronic portal hypertension was examined by use of the rat portal vein stenosis model. Intestinal blood flow and splenic pulp pressure were increased, while systemic arterial pressure and total vascular resistance were reduced in portal vein-stenosed rats as compared with controls. The reduction in total vascular resistance was entirely due to a fall in precapillary resistance and was accompanied by an increase in intestinal capillary pressure, which exceeded that produced by acute portal pressure elevation to the same level. Arteriovenous shunting of 15-micron microspheres was four times higher in portal-hypertensive rats. Cross-perfusion of control intestinal preparations with arterial blood from portal-hypertensive rats produced a 30% increase in blood flow. Plasma glucagon levels in portal-hypertensive rats were three times higher than in controls. Intra-arterial infusion of glucagon (at a rate that achieved the concentration measured in portal-hypertensive animals) produced a 20% reduction in intestinal vascular resistance. The results of these studies indicate that humoral factors, including glucagon, are primarily responsible for the hyperemia associated with portal hypertension.

Animals↗

PubMed1983

Restricted transport of cationic macromolecules across intestinal capillaries.

The charge-selective properties of intestinal capillaries were investigated by measuring steady-state lymph-to-plasma concentration ratios (L/P) of endogenous and exogenous macromolecules of comparable molecular size but different charge. The steady-state L/P values for endogenous lactate dehydrogenase isoenzymes (LD1-LD5) decreased with increasing isoelectric point. The osmotic reflection coefficient for LD1, the most negative isoenzyme studied, was 0.71 +/- 0.01; that for the most positive isoenzyme (LD5) was 0.95 +/- 0.01. The steady-state L/P for an exogenous molecule, neutral dextran, was 0.51 +/- 0.04; the L/P for the positively charged dextran of similar size was 0.25 +/- 0.04. The results indicate that intestinal capillaries behave as a positively charged barrier that reduces blood-lymph exchange of cationic macromolecules and enhances the exchange of anionic molecules.

Animals↗

PubMed1975