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AJP - Heart and Circulatory Physiology, Vol 272, Issue 2 728-H734, Copyright © 1997 by American Physiological Society
ARTICLES |
J. S. Jin and H. G. Bohlen
Department of Physiology and Biophysics, Indiana University Medical School, Indianapolis 46202, USA.
Release of nitric oxide from small arteries and larger arterioles of the intestine maintains their dilation and thereby supports mucosal blood flow. This flow-dependent mechanism can be studied by isosmotic replacement of sodium chloride with mannitol over the mucosa to lower mucosal metabolism and blood flow requirements. We tested the hypothesis that flow-mediated regulation is impaired in the non-insulin-dependent Zucker fatty diabetic (ZFD) male rats because of their marginally impaired endothelium-dependent dilation. Furthermore, we determined whether the depressed acetylcholine dilation associated with acute hyperglycemia in normoglycemic Zucker (NZ) rats also impairs flow-mediated regulation. When mannitol replaced sodium chloride over the villi, intestinal blood flow decreased significantly (P < 0.05) less in ZFD (80.9 +/- 6.8% of control) than NZ rats (40.9 +/- 6.4% of control). After 300 mg/dl hyperglycemia for 30 min, normal arterioles had impaired responses to acetylcholine and the resting blood flow and oxygen consumption were suppressed about 60%, which indicate the importance of basal nitric oxide release for intestinal vascular support of metabolism. The evidence of impaired flow-mediated dilation in ZFD and decreased resting blood flow after hyperglycemia in NZ rats demonstrated that both acute and chronic hyperglycemia disturb endothelial regulation of the intestinal vasculature.
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