AJP - Gastrointestinal and Liver Physiology, Vol 270, Issue 4 684-G690, Copyright © 1996 by American Physiological Society
Role of prostaglandins and nitric oxide in gastrointestinal hyperemia of diabetic rats
E. Goldin, M. Casadevall, M. Mourelle, I. Cirera, J. I. Elizalde, J. Panes, R. Casamitjana, P. Guth, J. M. Pique and J. Teres
Gastroenterology Department, Hospital Clinic, University of Barcelona, Spain.
The aim of the study was to characterize the gastric and mesenteric
vascular changes induced by diabetes and the implication of endothelial
[nitric oxide (NO) and prostaglandins] and humoral (glucagon) factors in
such changes. Diabetes was induced in rats by a single streptozotocin
injection. Four weeks later, gastric mucosa, left gastric artery, and
superior mesenteric artery blood flows were measured using hydrogen gas
clearance and perivascular ultrasonic flowmeter techniques, respectively,
in anesthetized and fasted diabetic and control rats. Blood pressure,
hematocrit, blood volume, and blood viscosity were also measured. Left
gastric (41 +/- 6 vs. 25 +/- 4 ml.min-1.100 g-1) and superior mesenteric
artery blood flows (83 +/- 8 vs. 65 +/- 4 ml.min-1.100 g-1) were
significantly higher in diabetic than in control rats. The increased blood
flow in the left gastric artery was distributed to a hypertrophic mucosa in
diabetic rats; therefore, the blood flow per 100 g tissue in the gastric
mucosa was not significantly different in diabetic compared with control
rats. Pretreatment with indomethacin reduced both increase gastric and
mesenteric flows of the diabetic rats to the same levels as in control
rats. NG-nitro-L-arginine methyl ester decreased gastric blood flow in a
dose-dependent manner and to a similar extent in diabetic and control rats.
In contrast, an increased sensitivity to the higher doses of the NO
inhibitor was observed in the mesenteric vascular bed of diabetic rats.
Glucagon reduction achieved by somatostatin infusion did not influence
either gastric or mesenteric blood flow in diabetic rats. In summary, the
present study revealed an increase in gastric and mesenteric arterial blood
flows in streptozotocin-induced diabetic rats. The gastrointestinal
hyperemia seems to be due, at least in part, to the increased demand of a
hypertrophic mucosa and is mediated primarily by endogenous prostaglandins.
Increased vascular sensitivity to NO may also contribute to the mesenteric
vasodilation.
