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Am J Physiol Heart Circ Physiol (June 19, 2003). doi:10.1152/ajpheart.00808.2002
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Submitted on September 13, 2002
Accepted on May 27, 2003

Influence of Peroxynitrite on Energy Metabolism and Cardiac Function in a Rat Ischemia-Reperfusion Model

Warren H Lee1, John S Gounarides2, Eric S Roos2, and Michael S Wolin3*

1 Department of Metabolic Cardiovascular Diseases, Novartis Institute for Biomedical Research, Summit, NJ, USA; Department of Physiology, New York Medical College, Valhalla, NY, USA
2 Department of Central Technologies, Novartis Institute for Biomedical Research, Summit, NJ, USA
3 Department of Physiology, New York Medical College, Valhalla, NY, USA

* To whom correspondence should be addressed. E-mail: mike_wolin{at}nymc.edu.

Ischemia-reperfusion (I/R) generates peroxynitrite (ONOO-), which interacts with many of the systems altered by I/R. This study examines the influence of endogenously produced ONOO- on cardiac metabolism and function. Nitro-L-arginine (an inhibitor of ONOO-, biosynthesis) and urate (a scavenger of ONOO-) were utilized to investigate potential pathophysiological roles for ONOO- using a rat Langendorff heart model perfused with glucose-containing saline at constant pressure, and exposed to 30 min of ischemia followed by 60 min of reperfusion. In this model, I/R decreased contractile function (e.g., left ventricular developed pressure, LVDP), cardiac work (rate-pressure product), efficiency of oxygen utilization, membrane bound creatine kinase activity, and NMR-detectable ATP and creatine phosphate, without significantly altering the recovery of coronary flow, heart rate, lactate release, and muscle pH. Urate and nitro-L-arginine produced a substantial recovery of LVDP, the rate-pressure product, efficiency of oxygen utilization, creatine kinase activity, NMR-detectable creatine phosphate, and a partial recovery of ATP. The pattern of effects observed in this study and in previously published work with similar models suggests that ONOO- may alter key steps in the efficiency of mitochondrial high-energy phosphate generation.




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