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Role of L-arginine-nitric oxide pathway in myocardial reoxygenation injury

Role of L-arginine-nitric oxide pathway in myocardial reoxygenation injury have increased the use of cardiopulmonary bypass (CPB) extracorporeal membrane oxygenation (ECMO) during infancy childhood (2, 13, 20). Clinical reports have described dysfunction either after correction of congenital heart disease on CPB (15) or during the treatment of pulmonary failure on ECMO (18). This study tests the hypothesis that the institution of either CPB or ECMO causes an immediate to the infantile, hypoxic heart subsequent alterations in cardiac contractility. The hypothesis is supported by the observations of de1 Nido et al. (8) that cyanotic infants undergoing on CPB had an increased content of conjugated dienes in their biopsies supported by a report of reduced systolic function in hypoxemic newborns placed on ECMO (18). To investigate the biochemical mechanisms responsible for the to the hypoxic heart during , we used an in vivo piglet H616 0363-6135/92 $2.00 This chemical reaction may be viewed as an alternate pathway of HO* generation during tissue is consistent with the known protective effects of super dismutase (1, 16). This investigation tests the hypothesis that in vivo of the infantile, hypoxic heart may be mediated, at least in part, by the L-arginine-NO pathway leading to the formation of peroxynitrite anion (ONOO-) HO.. METHODS Twenty-five http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Heart and Circulatory Physiology The American Physiological Society

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Publisher
The American Physiological Society
Copyright
Copyright © 1992 the American Physiological Society
ISSN
0363-6135
eISSN
1522-1539
Publisher site
See Article on Publisher Site

Abstract

have increased the use of cardiopulmonary bypass (CPB) extracorporeal membrane oxygenation (ECMO) during infancy childhood (2, 13, 20). Clinical reports have described dysfunction either after correction of congenital heart disease on CPB (15) or during the treatment of pulmonary failure on ECMO (18). This study tests the hypothesis that the institution of either CPB or ECMO causes an immediate to the infantile, hypoxic heart subsequent alterations in cardiac contractility. The hypothesis is supported by the observations of de1 Nido et al. (8) that cyanotic infants undergoing on CPB had an increased content of conjugated dienes in their biopsies supported by a report of reduced systolic function in hypoxemic newborns placed on ECMO (18). To investigate the biochemical mechanisms responsible for the to the hypoxic heart during , we used an in vivo piglet H616 0363-6135/92 $2.00 This chemical reaction may be viewed as an alternate pathway of HO* generation during tissue is consistent with the known protective effects of super dismutase (1, 16). This investigation tests the hypothesis that in vivo of the infantile, hypoxic heart may be mediated, at least in part, by the L-arginine-NO pathway leading to the formation of peroxynitrite anion (ONOO-) HO.. METHODS Twenty-five

Journal

AJP - Heart and Circulatory PhysiologyThe American Physiological Society

Published: Feb 1, 1992

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