Inhibition of nitric oxide limits infarct size in the in situ rabbit heart.
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 NG-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.
Patel
V C
VC
Hatter Institute for Cardiovascular Studies, Department of Academic Cardiology, University College London Medical School, UK.
Yellon
D M
DM
Singh
K J
KJ
Neild
G H
GH
Woolfson
R G
RG
D000704:Analysis of Variance; D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives* / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects; D006339:Heart Rate / Q000187:drug effects; D008297:Male; D009203:Myocardial Infarction / Q000503:physiopathology / Q000517:prevention & control*; D017202:Myocardial Ischemia / Q000503:physiopathology; D015425:Myocardial Reperfusion; D019331:NG-Nitroarginine Methyl Ester; D009569:Nitric Oxide / Q000037:antagonists & inhibitors*; D011817:Rabbits
D009569:Nitric Oxide; D001120:Arginine; D019331:NG-Nitroarginine Methyl Ester