Non-insulin dependent diabetes and hyperglycemia impair rat
intestinal flow mediated regulation.
Jin, Jong-Shiaw, and H. Glenn Bohlen.
Department of Physiology and Biophysics, Indiana University Medical
School, Indianapolis, IN 46202
APStracts 3:0381H, 1996.
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
isosomotic replacement of NaCl 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 male (ZFD) rats because of
their marginally impaired endothelium dependent dilation. Further, we
determined if the depressed acetylcholine dilation associated with
acute hyperglycemia in normoglycemic Zucker rats (NZ) also impairs
flow mediated regulation. When mannitol replaced NaCl 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
indicates 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 following
hyperglycemia in NZ rats demonstrated both acute and chronic
hyperglycemia disturb endothelial regulation of the intestinal
vasculature.
Received 13 May 1996; accepted in final form 22 August 1996.
APS Manuscript Number H424-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 19 September 1996