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Biomedical subjects

K M Walus

Publications and source records attributed to K M Walus.

9 recordsLinked to original sources
PubMed1981

Hemodynamic and metabolic changes during stimulation of ileal motility.

Hemodynamic and metabolic responses of the mesenteric circulation were studied during infusion of agents known to stimulate intestinal motility. Agents were infused intraarterially in graded doses and included acetylcholine, angiotensin II, prostaglandin D2, prostaglandin F2-alpha, methionine-enkephalin, and morphine. Measurements were made of blood flow to the ileal portion of the small intestine, arteriovenous oxygen content difference, fractional distribution of radiolabeled microspheres to the muscularis, and intraluminal pressure. The clearance of 86Rb was determined in some experiments. From these measurements we calculated oxygen consumption, fractional blood flow to the muscularis, permeability and surface area product (PS-product), and the mean motility index. All agents increased mean motility index to varying degrees. At comparable levels of increased mean motility index with each drug, there were variable degrees of increase or decrease or no change in the other parameters between drugs. Mesenteric hemodynamic and metabolic responses to these dissimilar stimuli of motor activity reflected mainly the vasoactive properties of each agent. This suggests that increased motor activity has little influence on the mesenteric circulation.

Acetylcholine↗
PubMed1981

Mesenteric vascular reactivity to histamine receptor agonists and antagonists.

Response patterns of intestinal blood flow, oxygen extraction and consumption, blood flow distribution, and motility were assessed during intraarterial infusions of histamine, histamine after H1 or H2 blockade, dimaprit or dimaprit after H2 blockade. Histamine produced an initial peak response of blood flow with a slow decrease thereafter. Oxygen extraction was evenly depressed throughout the infusion, and oxygen consumption increased at the beginning. All initial responses were blocked by tripelennamine. Ranitidine, a new H2 antagonist, accelerated the decay of all responses. Dimaprit produced effects identical to those of histamine after tripelennamine. Distribution of blood flow was unchanged at the beginning of histamine infusion, but subsequently showed a shift to muscularis which was blocked by tripelennamine. Histamine usually stimulated intestinal contractions and this effect was abolished by tripelennamine. Thus, H1 stimulation, besides producing an initial vasodilation, increases oxygen uptake and redistributes flow to the muscularis.

Adrenergic Agonists↗
PubMed1981

Gastrointestinal secretory, motor, circulatory, and metabolic effects of prosomatostatin.

This study compares the gastrointestinal effects of somatostatin (SS) and its putative prohormone, prosomatostatin (Pro-SS), a 28-amino acid peptide isolated from the hypothalamus and the gut, in conscious dogs with chronic gastric and pancreatic fistulae. Pro-Ss suppressed the release of serum gastrin, insulin, and pancreatic polypeptide that occurs in response to feeding a meat meal in a manner similar to that seen with SS. However, in contrast to SS, which strongly reduced intestinal blood flow and oxygen consumption and stimulated intestinal motility, Pro-SS, at the doses tested, had no influence on mesenteric circulation, oxygen uptake, and intestinal motility. We conclude that Pro-SS mimics most of the gastrointestinal secretory actions of SS, but does not exhibit the intestinal circulatory, metabolic, and motor effects of SS.

Animals↗
PubMed1981

Relation between small intestinal motility and circulation.

Effects of muscular activity on local blood flow have been delineated in other muscular organs but are part of a complex relationship in the small intestine. Some of our inability to provide a clear picture of the circulatory events surrounding intestinal motility relates to the variety of imprecise techniques that have been used to explore the relationship. Distension of the gut impedes blood flow through the intestinal wall, especially in the mucosa. Stimulation of motility evokes more variable responses in the intestinal circulation, including increases in blood flow; however, the circulatory response reflects mostly the nature of the intervention used to activate motility. Many motor stimuli in the gut have intrinsic vasoactive properties. Spontaneous motor events seem to have only small effects on total blood flow to the small intestine. Reduction in blood flow to the gut evokes initial increases in motility followed by inhibition of motor activity. Products of metabolism in the intestine influence both motor and vascular reactivity. More sensitive methods need to be developed to separate the types of intestinal motor activity, to localize mechanical events in specific sites in the wall of the gut, to better record electrical correlates of motility, and to measure local tissue blood flow. These technical developments will permit delineation of the linkage between motor and vascular events and should identify the regulatory factors.

Animals↗
PubMed1981

Effects of calcium and its antagonists on the canine mesenteric circulation.

We studied circulatory and metabolic responses of the intestinal circulation to intraarterial infusions of solutions containing calcium chloride or calcium antagonists in anesthetized dogs. Measurements included blood flow to the terminal ileum, arteriovenous oxygen content difference, distribution of radiolabeled microspheres to the mucosal-submucosal compartment and intraluminal pressure. Calculated parameters included oxygen consumption and fractional mucosal-submucosal blood flow. Both calcium antagonists, nifedipine and diltiazem, increased intestinal blood flow, mainly to the mucosa-submucosa, depressed intestinal motility, and did not change oxygen consumption. Thus, both agents appear to act mainly on resistance vessels without increasing the nutrient circulation. Calcium chloride (1.0-500.0 microgram/kg per min) had a mild constrictor effect; at a dose of 1000.0 microgram/kg per min, calcium chloride became a dilator agent in the mesenteric circulation. The dilator effect of the highest dose of calcium was reversed by digoxin, suggesting the involvement of Na+,K+-ATPase. Nifedipine completely blocked calcium-induced constriction of the intestinal circulation and partly inhibited norepinephrine-induced constriction. Studies on isolated mesenteric arterial smooth muscle revealed that nifedipine relaxed KCl-contracted strips in the presence of external calcium and relaxed norepinephrine-contracted strips in both the presence and absence of external calcium. These in vitro findings suggest that calcium antagonists interfere with the release of calcium from intracellular sites as well as with the slow inward current of calcium.

Animals↗
PubMed1981

Effects of adenosine and its derivatives on the canine intestinal vasculature.

The effects of adenosine and two of its structural analogs on small intestinal blood flow, flow distribution, oxygen extraction, and uptake were studied in anesthetized dogs. Adenosine induced dose-dependent increases in intestinal blood flow and oxygen consumption but decreased oxygen extraction. These effects were significantly attenuated by theophylline, an adenosine antagonist. Propranolol did not influence the responses of the intestinal circulation to adenosine suggesting that beta-adrenergic receptors are not involved in the action of adenosine. 2-Chloroadenosine, one of the most potent adenosine analogs, produced changes very similar to adenosine but was about six times more potent on a molar basis. Effects of 2-chloroadenosine were attenuated by a 10-fold smaller dose of theophylline. Adenosine-9 beta-D-arabinofuranoside, another analog, was ineffective in the mesenteric circulation. Characteristic activity of both analogs and the antagonism of the effects of adenosine and 2-chloroadenosine by theophylline suggest the presence of adenosine-sensitive binding sites in precapillary resistance vessels of the intestinal circulation. The presence of adenosine receptors in intestinal vascular smooth muscle is further supported by our in vitro results in which all three agents induce patterns of response similar to those noted under in vivo conditions. However, concentrations necessary to obtain relaxation of isolated muscle strips were much greater than those sufficient to produce mesenteric vasodilation in vivo. It was also noted that strips obtained from branches of the superior mesenteric artery were more reactive to adenosine and its analogs than were strips prepared from the main trunk of the vessel.

Adenosine↗
PubMed1980

Differential effects of prostaglandins and arachidonic acid on gastric circulation and oxygen consumption.

Experiments were carried out on anesthetized dogs to compare the effects of prostaglandin E2 (PGE2), prostacyclin (PGI2) and arachidonic acid (AA) administered intraarterially on gastric blood flow and oxygen consumption during constant arterial pressure perfusion and constant flow perfusion of the stomach. Both PGE2 and PGI2 increased total blood flow and oxygen consumption both in the resting stomach and following histamine stimulation although the effects of PGE2 on the oxygen consumption in stimulated stomach were not statistically significant. On the contrary, AA decreased both gastric blood flow and oxygen consumption in the histamine stimulated stomach. To determine if these compounds can influence gastric oxygen consumption independently of their effects on blood flow, the experiments with constant flow perfusion were performed. Both PGE2 and PGI2 decreased both the perfusion pressure and oxygen consumption in the resting as well as in the histamine-stimulated stomach whereas AA increased perfusion pressure and decreased oxygen consumption during histamine administration. Effects of AA were blocked by indomethacin suggesting that not AA itself but some of its metabolites, most likely thromboxanes were responsible for the hemodynamic and metabolic changes resulting from the contraction of gastric arterioles and precapillary sphincters. On the contrary, both PGE2 and PGI2 caused gastric hyperemia and an increase in oxygen consumption in the resting stomach, but decreased the latter parameter in the stimulated stomach, most probably as a result of secretory inhibition overcoming direct vascular effects of these compounds.

Animals↗