INHIBITION OF NITRIC-OXIDE LIMITS INFARCT SIZE IN THE IN-SITU RABBIT HEART

被引：167

作者：

PATEL, VC

YELLON, DM

SINGH, KJ

NEILD, GH

WOOLFSON, RG

机构：

[1] UCL, SCH MED,DEPT ACAD CARDIOL, HATTER INST CARDIOVASC STUDIES,GOWER ST, LONDON WC1E 6AU, ENGLAND

[2] UCL, SCH MED, INST UROL & NEPHROL, DEPT NEPHROL, LONDON WC1E 6AU, ENGLAND

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 1993年 / 194卷 / 01期

关键词：

D O I：

10.1006/bbrc.1993.1809

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Recent data has suggested a dual role for nitric oxide (NO) so that it can both attenuate myocardial injury during ischaemia and reperfusion as well as mediate reperfusion injury. In this study in the in situ rabbit heart, we have shown that pretreatment with intravenous N(G)-nitro-L-arginine methyl ester (L-NAME, an inhibitor of NO synthesis) significantly reduced infarct size following sustained coronary artery occlusion and reperfusion. L-NAME was also noted to increase myocardial lactate concentration. This study provides further evidence that protection against ischaemia-reperfusion injury can be derived from manipulation of the microcirculation. © 1993 Academic Press, Inc.

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页码：234 / 238

页数：5

相关论文

共 18 条

[1] APPARENT HYDROXYL RADICAL PRODUCTION BY PEROXYNITRITE - IMPLICATIONS FOR ENDOTHELIAL INJURY FROM NITRIC-OXIDE AND SUPEROXIDE [J].

BECKMAN, JS ;

BECKMAN, TW ;

CHEN, J ;

MARSHALL, PA ;

FREEMAN, BA .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1990, 87 (04) :1620-1624

[2] THE NEUROPROTECTIVE EFFECT OF A NITRIC-OXIDE INHIBITOR IN A RAT MODEL OF FOCAL CEREBRAL-ISCHEMIA [J].

BUISSON, A ;

PLOTKINE, M ;

BOULU, RG .

BRITISH JOURNAL OF PHARMACOLOGY, 1992, 106 (04) :766-767

[3] INTERFERON-GAMMA AND TUMOR-NECROSIS-FACTOR SYNERGIZE TO INDUCE NITRIC-OXIDE PRODUCTION AND INHIBIT MITOCHONDRIAL RESPIRATION IN VASCULAR SMOOTH-MUSCLE CELLS [J].

GENG, Y ;

HANSSON, GK ;

HOLME, E .

CIRCULATION RESEARCH, 1992, 71 (05) :1268-1276

[4] NITRIC-OXIDE - A CYTO-TOXIC ACTIVATED MACROPHAGE EFFECTOR MOLECULE [J].

HIBBS, JB ;

TAINTOR, RR ;

VAVRIN, Z ;

RACHLIN, EM .

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1988, 157 (01) :87-94

[5]

HOHORST HJ, 1963, METHOD ENZYMAT AN, P266

[6]

JOHNSON G, 1990, J PHARMACOL EXP THER, V252, P35

[7] ROLE OF NITRIC-OXIDE IN REACTIVE HYPEREMIA OF THE GUINEA-PIG HEART [J].

KOSTIC, MM ;

SCHRADER, J .

CIRCULATION RESEARCH, 1992, 70 (01) :208-212

[8] PROTECTION AGAINST INFARCTION AFFORDED BY PRECONDITIONING IS MEDIATED BY A1 ADENOSINE RECEPTORS IN RABBIT HEART [J].

LIU, GS ;

THORNTON, J ;

VANWINKLE, DM ;

STANLEY, AWH ;

OLSSON, RA ;

DOWNEY, JM .

CIRCULATION, 1991, 84 (01) :350-356

[9] DIMINISHED BASAL NITRIC-OXIDE RELEASE AFTER MYOCARDIAL-ISCHEMIA AND REPERFUSION PROMOTES NEUTROPHIL ADHERENCE TO CORONARY ENDOTHELIUM [J].

MA, XL ;

WEYRICH, AS ;

LEFER, DJ ;

LEFER, AM .

CIRCULATION RESEARCH, 1993, 72 (02) :403-412

[10] ROLE OF L-ARGININE-NITRIC OXIDE PATHWAY IN MYOCARDIAL REOXYGENATION INJURY [J].

MATHEIS, G ;

SHERMAN, MP ;

BUCKBERG, GD ;

HAYBRON, DM ;

YOUNG, HH ;

IGNARRO, LJ .

AMERICAN JOURNAL OF PHYSIOLOGY, 1992, 262 (02) :H616-H620