Ischemia/reperfusion increases gastric motility and endothelin-1
-induced vasoconstriction.
Wood, J. G., Z. Y. Yan, Q. Zhang, and L. Y. Cheung.
Departments of Surgery and Physiology, University of Kansas Medical
Center, Kansas City, KS 66160
APStracts 2:0079G, 1995.
The purpose of our study was to: 1) examine the effect of
ischemia/reperfusion on gastric vascular resistance (GVR) and
motility, 2) determine whether endothelin-1-(ET-1)-induced vasocon
striction is enhanced following ischemia/reperfusion, and 3) assess
the effect of superoxide dismutase (SOD) on these alterations. These
experiments used a mechanically-perfused ex vivo gastric segment of
chloralose-anesthetized dogs. We first evaluated the effect of
varying the duration of total ischemia on reperfusion-induced changes
in GVR and motility. Responses to ET-1 (10-10 M) were compared prior
to and after 30 min ischemia/30 min reperfusio n, with saline or SOD
(10 U/ml) infused i.a. to the stomach during reperfusion. We found
that: 1) after ischemia, vasodilation occurs initially upon
reperfusion followed by a progressive increase in GVR, 2) contractile
force was reduced during ischemia, but elevated upon reperfusion, 3)
vasoconstrictor responses to ET-1 were enhanced after
ischemia/reperfusion, and 4) SOD reduced the enhanced response to ET
-1 and contractile force. Our findings support the hypothesis that
reactive oxygen metabolites contribute to augmented vascular
reactivity and hypercontractility following ischemia/reperfusion.
Received 2 December 1994; accepted in final form 19 April 1995,
APS Manuscript Number G474-4.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 2 May 1995.