Biomedical subjects

R A Nyhof

Publications and source records attributed to R A Nyhof.

7 recordsLinked to original sources

PubMed1985

Effect of atropine on digested food-induced intestinal hyperemia.

The aim of our study was to determine whether the discrepancy in the data reported on the effect of atropine on food-induced intestinal hyperemia results from a difference in experimental materials and methods. In the first two series of experiments, atropine (0.5 mg/kg iv) was given before or during intraluminal perfusion of digested food plus bile through a long jejunal loop (62% of the total small intestine) at 4 ml/min for 60 min while measuring the portion of the blood flow through the superior mesenteric artery (SMA) that perfused the loop. Atropine per se had no effect on jejunal blood flow. Before atropine food increased flow 31.5 +/- 10.1% and after atropine flow increased 54.8 +/- 11.0 and 66.0 +/- 28.0% above controls in the first and second series, respectively. Atropine also increased net fluid volume absorption. In the third series, food alone and food plus bile were placed into the lumens of the two adjacent jejunal segments. Atropine had no effect on the increases in flow and oxygen uptake produced by food alone but enhanced the hyperemia produced by food plus bile without affecting the increase in oxygen uptake. Our results suggest that the previously reported inhibition of increased SMA flow by atropine is due to the inhibitory effect of atropine on gastrointestinal motility and inhibition of pancreatic blood flow. In conclusion, food-induced jejunal hyperemia does not result from a direct vasodilator action of the cholinergic nerves.

Animals↗

PubMed1985

Regulation of jejunal blood flow and oxygenation during glucose and oleic acid absorption.

To differentiate the mechanisms whereby actively absorbed glucose and passively absorbed oleic acid increase blood flow and oxygen uptake during their absorption, the effects of these two nutrients on jejunal blood flow, arteriovenous oxygen difference [(a-v)O2], O2 uptake, absorption, rubidium extraction, and capillary permeability-surface area product (PS) were compared in anesthetized dogs. Oleic acid (37 mM) produced significantly greater hyperemia (+28.2%) than glucose (270 mM) did (+12.5%). As estimated by (a-v)O2, tissue oxygen extraction was decreased by oleic acid (-12%) but increased by glucose (+6.5%); the increases in O2 uptake by these two nutrients did not differ significantly. Glucose absorption was accompanied by an increase in rubidium extraction and capillary PS (+11.3%), whereas oleic acid absorption was not. Unlike glucose, intra-arterial infusion of oleic acid decreased vascular resistance and increased blood flow equally to the mucosa and muscularis layers. A significant relation existed between oleic acid absorption and blood flow but not between glucose absorption and blood flow. The enhancement of glucose-induced hyperemia by bile was not related to glucose absorption. Unmasking of oleic acid-induced hyperemia by bile is unrelated to oleic acid absorption but is related to solubility of oleic acid in aqueous solution. The above findings suggest that glucose absorption affects both resistance and exchange vessels, whereas oleic acid absorption affects primarily resistance vessels.

Animals↗

PubMed1984

Central and regional hemodynamics during the acute onset of renal hypertension in rats.

The purpose of this study was to quantitate the regional changes in flow and resistance which occur during the acute onset of two-kidney, one clip renal hypertension. Anesthetized rats were implanted with a Doppler flow probe and balloon occluder on one renal artery. To produce acute hypertension, the occluder was inflated to reduce renal flow velocity by 50%. After 90 minutes, mean arterial pressure increased 25% above the prestenosis control period value as a result of a 22% increase in peripheral resistance. Regional flows and resistances were determined prior to and 90 minutes after renal artery stenosis by injection of labelled microspheres into the left ventricle. Our major findings were that: 1) the regional hemodynamic changes in flow and resistance are unevenly distributed among individual organs; and 2) the major site of increased resistance resides in the splanchnic circulation with the largest increases occurring in the small intestine.

Animals↗

PubMed1983

Evidence against local neural mechanism for intestinal postprandial hyperemia.

The role of local intestinal nerves in the nutrient-induced intestinal hyperemia was investigated in jejunal segments of anesthetized dogs by comparing the hyperemic effect of intraluminal glucose and oleic acid solutions before and after mucosal anesthesia and infusions of methysergide, hexamethonium, and tetrodotoxin. Methysergide, hexamethonium, and tetrodotoxin all failed to alter either the vascular or metabolic responses to luminal placement of glucose or oleic acid. The increases in blood flow and oxygen uptake produced by glucose or oleic acid, however, were blocked or attenuated after exposing the mucosa to dibucaine. The effect was norepinephrine due to an altered vascular response to vasoactive substances as dibucaine did not alter vascular responses to isoproterenol or norepinephrine. Dibucaine, however, inhibited active transport and increased passive transport of glucose across rat intestinal sacs in vitro. Oxygen consumption of the canine jejunal mucosa was also inhibited by dibucaine in vitro. It seems that inhibition of the nutrient-induced intestinal hyperemia by dibucaine is due, at least in part, to its effect on oxygen consumption and glucose transport of the mucosal epithelial cells. Nutrient-induced hyperemia appears not to be neurally mediated but more closely related to metabolism.

Animals↗

PubMed1983

Splanchnic circulation in hypertension.

The effect of arterial hypertension on the splanchnic circulation is assessed. In human essential hypertension, splanchnic vascular resistance rises in proportion to the blood pressure, and the transvascular escape rate of plasma proteins is increased. The various animal models of hypertension show variable results, but in general support the concept that vascular resistance changes in the splanchnic organs are similar in direction and magnitude to pressure changes. This is especially true in longer-term chronic experiments. These resistance changes appear to result from increased responsiveness of the arterioles to a variety of constrictor influences, and they may result from either structural or functional changes. Hypertension appears to alter splanchnic arteriolar permeability via a pressure-dependent mechanism. These vessels may also undergo degenerative histological changes. Capillaries and small venules experience increased endothelial permeability via a pressure-independent mechanism that is not mediated by angiotensin II. In addition to the resistive and exchange alterations, the capacitance function of splanchnic veins is reduced, probably via a structural change. Much work remains to be done before the characterization is complete. Especially needed are studies of individual organs with respect to vascular resistance, exchange, and capacitance alterations in the various models of hypertension.

Animals↗

PubMed1982

Dynamics of intestinal oxygenation: interactions between oxygen supply and uptake.

The oxygenation of intestinal tissue is dependent on the interaction of three distinctive transport processes: 1) convection (i.e., blood flow), 2) diffusion, and 3) chemical reaction. Oxygen is transported to the capillary level by convection. Local adjustments of blood flow in accordance with tissue oxygen demand serve to stabilize capillary oxygen tension. After reaching the capillary, oxygen is transferred into the parenchymal cells by diffusion. Intrinsic modulation of the number of perfused capillaries allows vascular control of exchange surface area and effective capillary-to-cell diffusion distance. On entering the cell, molecular oxygen acts as the electron acceptor responsible for maintaining continuous mitochondrial respiration and the interlinked oxidative formation of ATP. The basic interaction of blood flow, diffusion, and mitochondrial respiration under a variety of conditions are illustrated utilizing a simplified graphic approach. The analysis demonstrates the ability of the flow and exchange controllers, operating in unison, to provide a wide margin of safety against development of cell hypoxia under a variety of stresses. Finally, the role of oxygen, adenosine, and prostaglandins as possible mediators of intrinsic vasoregulation in intestine is discussed.

Animals↗

PubMedDate not supplied

Acute local effects of angiotensin II on the intestinal vasculature.

The vasotoxic properties of angiotensin II (AII) on vascular endothelial cells have been implicated in the increased extravasation of proteins and water observed in certain forms of chronic arterial hypertension. Since microvascular permeability in the small intestine is increased in one-kidney, one clip hypertension, we tested the hypothesis that AII decreases the permselectivity of intestinal microvessels to plasma proteins. The acute intestinal vascular effects of AII were studied by locally infusing AII into isolated canine jejunal segments. A measure of vascular permeability in control and infused segments was obtained by estimating the osmotic reflection coefficient as 1-lymph/plasma protein concentration ratio when the ratio reached a plateau at high lymph flows. Lymph flows were increased by raising the venous pressure from a control of 5 to 30-35 mm Hg in 5 mm Hg steps. Resting control blood and lymph flows were reduced by AII, but these flows were not different at the higher venous pressures due to the apparent blunting of the venous-arteriolar response by AII. The estimated osmotic reflection coefficient of 0.85 for the control animals was less than that obtained in the infused segments (0.93). This effect was substantiated by electrophoretic separation of protein fractions. Thus, AII per se does not cause an acute increase in intestinal vascular permeability, and may, in fact reduce it.

Angiotensin II↗