Heat shock protein induction inhibits inducible nitric oxide
synthase mrna expression and attenuates hypotension in endotoxin
-challenged rats.
Hauser, Gabriel J., Emmanuel K. Dayao, Karla Wasserloos, Bruce R.
Pitt, and Hector R. Wong.
Division of Pediatric Critical Care Medicine, Georgetown University
Children's Medical Center, and Department of Physiology and
Biophysics, Georgetown University, Washington, DC 20007, University
of Pittsburgh School of Medicine, Pittsburgh, PA, 15217, and Division
of Critical Care Medicine, Children's Hospital Medical Center,
Cincinnati, OH 45229
APStracts 3:0233H, 1996.
Endotoxin (LPS)-induced hypotension is, in part, mediated via
induction of nitric oxide synthase (iNOS), release of nitric oxide
(NO), and suppression of vascular reactivity (vasoplegia). Induction
of heat shock proteins (HSPs) or inhibition of iNOS expression
improve survival in LPS-challenged rodents. We studied the effect of
induction of heat shock proteins on LPS-mediated iNOS expression, and
on LPS-induced vasoplegia and hypotension.
Received 14 December 1995; accepted in final form 22 May 1996.
APS Manuscript Number H1173-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 17 June 96