© 1997 by European Society of Cardiology
Copyright © 1997, European Society of Cardiology
Generation of peroxynitrite contributes to ischemia-reperfusion injury in isolated rat hearts
Departments of Pediatrics and Pharmacology, Cardiovascular Disease Research Group, 462 Heritage Medical Research Centre, University of Alberta, Edmonton, Alta. T6G 2S2, Canada
Objective: The acute release of radicals upon reperfusion following myocardial ischemia may include both nitric oxide (NO) and superoxide anion (O2–•). The generation of peroxynitrite (ONOO–) from these radicals may contribute to ischemia-reperfusion injury. Our objective was to measure the generation of ONOO– during reperfusion of isolated hearts subjected to ischemia and to determine the effects of inhibition of NO synthase with NG-monomethyl-L-arginine (L-NMMA), or supplementation of NO with S-nitroso-N-acetyl-D,L-penicillamine (SNAP), on ONOO– generation and on the recovery of mechanical function. Methods and Results: Isolated rat hearts were perfused at constant pressure with Krebs' buffer containing L-tyrosine, which reacts with ONOO– to form dityrosine, a fluorescent product. Dityrosine was detected in the coronary effluent of hearts infused with synthetic ONOO–. In hearts subjected to 20 min of global, no-flow ischemia there was a marked rise in endogenous ONOO– formation which peaked at 30 s of reperfusion. Formation of ONOO– was dependent upon synthesis of both NO and O2–•, as dityrosine release was abolished by L-NMMA or superoxide dismutase, respectively. L-NMMA caused a concentration-dependent improvement in the recovery of mechanical function during reperfusion. Infusion of SNAP also abolished dityrosine release at reperfusion and improved the recovery of post-ischemic function. Conclusions: Our results show for the first time that reperfusion of the ischemic heart causes the acute production of ONOO–. Inhibiting the biosynthesis of ONOO– with L-NMMA or antagonizing its oxidant actions with SNAP are possible strategies to protect the heart from ischemia-reperfusion injury.
KEYWORDS NO, nitric oxide; NOS, NO synthase; SNAP, S-nitroso-N-acetyl-D,L-penicillamine; ONOO–, peroxynitrite; O2–•, superoxide anion; L-NMMA, NG-monomethyl-L-arginine
* Corresponding author. Tel. +1 403 492-6581; Fax +1 403 492-9753; E-mail: richard.schulz@ualberta.ca
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E. Mori, N. Haramaki, H. Ikeda, and T. Imaizumi Intra-coronary administration of L-arginine aggravates myocardial stunning through production of peroxynitrite in dogs Cardiovasc Res, October 1, 1998; 40(1): 113 - 113. [Abstract] [Full Text] [PDF]
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D. Panas, F. H. Khadour, C. Szabo, and R. Schulz Proinflammatory cytokines depress cardiac efficiency by a nitric oxide-dependent mechanism Am J Physiol Heart Circ Physiol, September 1, 1998; 275(3): H1016 - H1023. [Abstract] [Full Text] [PDF]
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R. Bolli, Z. A. Bhatti, X.-L. Tang, Y. Qiu, Q. Zhang, Y. Guo, and A. K. Jadoon Evidence That Late Preconditioning Against Myocardial Stunning in Conscious Rabbits Is Triggered by the Generation of Nitric Oxide Circ. Res., July 19, 1997; 81(1): 42 - 52. [Abstract] [Full Text]
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