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Influence of peroxynitrite on energy metabolism and cardiac function in a rat ischemia-reperfusion model

¹Metabolic Cardiovascular Diseases and ²Central Technologies, Novartis Institute for Biomedical Research, Summit, New Jersey 07901; and ³Department of Physiology, New York Medical College, Valhalla, New York 10595

Submitted 13 September 2002 ; accepted in final form 27 May 2003

Ischemia-reperfusion generates peroxynitrite (ONOO^–), which interacts with many of the systems altered by ischemia-reperfusion. 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^– in 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, ischemia-reperfusion decreased contractile function (e.g., left ventricular developed pressure), cardiac work (rate-pressure product), efficiency of O₂ 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. Treatment with urate and nitro-L-arginine produced a substantial recovery of left ventricular developed pressure, rate-pressure product, efficiency of O₂ utilization, creatine kinase activity, and 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.

urate; nitric oxide; oxygen consumption; reactive oxygen species; heart perfusion

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