© 1997 by European Society of Cardiology
Copyright © 1997, European Society of Cardiology
Peroxynitrite aggravates myocardial reperfusion injury in the isolated perfused rat heart
aDivision of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA 19107-5004, USA
bInstitute for Environmental Medicine, University of Pennsylvania, Philadelphia, PA 19104-6068, USA
* Corresponding author. Tel. (+1-215) 9556844; Fax (+1-215) 9236225.
Objective: This study examined the effects of peroxynitrite (ONOO–) on cardiac function and cellular injury following ischemia (30 min) and reperfusion (60 min) in isolated perfused rat hearts. Methods: 3-Morpholinosydnonimine (SIN-1, 0.1 mM), an ONOO– donor, was administered alone or combined with superoxide dismutase (SOD, 300 U/ml) or glutathione (GSH, 1 mM) at the time of reperfusion. Results: Administration of SIN-1 alone significantly aggravated post-ischemic myocardial injury characterized by depressed cardiac function recovery (p<0.05 vs. vehicle), increased lactic dehydrogenase (LDH) and creatine kinase (CK) release (p<0.01 vs. vehicle), and enlarged necrotic size (p<0.01 vs. vehicle). The co-administration of either SOD to decrease the formation of ONOO–, or GSH to increase the detoxification of ONOO–, completely blocked the detrimental effects of SIN-1 and exerted significant cardioprotective effects against reperfusion injury. Conclusion: These results suggest that ONOO– may play a significant role in postischemic myocardial injury.
KEYWORDS Peroxynitrite; Nitric oxide; Reperfusion injury
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