Role of prostaglandins and nitric oxide in the gastrointestinal
hyperemia of diabetic rats.
Goldin, Eran, Maria Casadevall, Marisa Mourelle, Isabel Cirera, Josep
I. Elizalde, Julian Pan[acute]es, Roser Casamitjana, Paul Guth, Josep
M. Piqu[acute]e, Josep Ter[acute]es.
Gastroenterology Department, Hospital Cl[acute]inic, University of
Barcelona, and Digestive System Research Unit, Hospital Vall
d'Hebron, Barcelona, Spain
APStracts 2:0223G, 1995.
The aim of the study was to characterize the gastric and mesenteric
vascular changes induced by diabetes and the implication of
endothelial (nitric oxide 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
flowmeters techniques respectively, in anesthetized, 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/100g) and superior mesenteric arteries blood flow (83+/-8 vs
65+/-4 ml/min/100g) 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 of tissue in the gastric mucosa was not
significantly different in diabetic as compared with control rats.
Pretreatment with indomethacin, reduced both increased 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 in 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.
Received 24 July 1995; accepted in final form 18 October 1995.
APS Manuscript Number G309-5.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 November 95