Preconditioning decreases ischemia/reperfusion-induced peroxynitrite formation

Biochem Biophys Res Commun. 2001 Aug 3;285(5):1217-9. doi: 10.1006/bbrc.2001.5308.


The role for peroxynitrite (ONOO(-)) in the mechanism of preconditioning is not known. Therefore, we studied effects of preconditioning and subsequent ischemia/reperfusion on myocardial ONOO(-) formation in isolated rat hearts. Hearts were subjected to a preconditioning protocol (three intermittent periods of global ischemia/reperfusion of 5 min duration each) followed by a test ischemia/reperfusion (30 min global ischemia and 15 min reperfusion). When compared to nonpreconditioned controls, preceding preconditioning improved postischemic cardiac performance and significantly decreased test ischemia/reperfusion-induced formation of free nitrotyrosine measured in the perfusate as a marker for cardiac endogenous ONOO(-) formation. During preconditioning, however, the first period of ischemia/reperfusion increased nitrotyrosine formation, which was attenuated after the third period of ischemia/reperfusion. We conclude that classic preconditioning inhibits ischemia/reperfusion-induced cardiac formation of ONOO(-) and that subsequent periods of ischemia/reperfusion result in a gradual attenuation of ischemia/reperfusion-induced ONOO(-) generation. This mechanism might be involved in ischemic adaptation of the heart.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Aorta
  • Blood Flow Velocity
  • In Vitro Techniques
  • Ischemic Preconditioning, Myocardial / methods*
  • L-Lactate Dehydrogenase / biosynthesis
  • Male
  • Myocardial Ischemia / physiopathology*
  • Myocardial Reperfusion Injury / prevention & control
  • Myocardial Reperfusion*
  • Myocardium / metabolism*
  • Nitrates / metabolism*
  • Rats
  • Rats, Wistar
  • Time Factors
  • Tyrosine / analogs & derivatives*
  • Tyrosine / biosynthesis
  • Ventricular Function, Left


  • Nitrates
  • peroxynitric acid
  • 3-nitrotyrosine
  • Tyrosine
  • L-Lactate Dehydrogenase