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Am J Physiol Gastrointest Liver Physiol 253: G26-G32, 1987;
0193-1857/87 $5.00
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AJP - Gastrointestinal and Liver Physiology, Vol 253, Issue 1 26-G32, Copyright © 1987 by American Physiological Society

ARTICLES

Intestinal hyperemia in experimental diabetes mellitus

R. J. Korthuis, J. N. Benoit, P. R. Kvietys, M. H. Laughlin, A. E. Taylor and D. N. Granger

Intestinal blood flows were measured using the radioactive microsphere technique in anesthetized, fasted (18-24 h) rats 4 wk after administration of streptozotocin (65 mg/kg body wt) or its vehicle. Blood flow was increased along the length of the small bowel in diabetic rats relative to normal animals. In an attempt to define the mechanisms underlying the intestinal hyperemic response to diabetes, we employed an in situ, blood perfused, isolated rat jejunum-ileum preparation. Intestinal blood flow was increased by 37%, while intestinal vascular resistance was reduced by 39% in diabetic rats relative to control animals. Cross-perfusion of control intestinal preparations with arterial blood from diabetic rats produced a 30% increase in blood flow and a 24% reduction in vascular resistance. Increasing plasma osmolarity, plasma glucose concentration, or plasma glucagon concentration in control animals to levels measured in diabetic animals produced reductions in vascular resistance that were qualitatively similar to that seen in the diabetic intestine. Intestinal vascular sensitivity to norepinephrine was assessed by constructing dose-response curves in control and diabetic animals. The mean ED50 values for norepinephrine were increased in diabetic rats relative to control animals. These results indicate that the intestinal hyperemic response in diabetes may be related to increased levels of circulating vasodilators, including hyperosmolarity and glucagon, and a reduced vascular sensitivity to norepinephrine.


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