Ischemic preconditioning decreases nitric oxide formation and nitric oxide mediated injury in the postischemic heart

Jay L. Zweier, Penghai Wang

Research output: Contribution to journalArticlepeer-review


Increased nitric oxide (NO) formation occurs during myocardial ischemia and is an important mediator of postischemic injury. However, the effect of ischemic preconditioning on subsequent NO formation and the importance of these alterations in myocardial protection are unknown. Therefore correlative studies of NO formation, and postischemic injury were performed in an isolated rat heart preconditioning model of 4 cycles of 5 min of ischemia followed by 30 min of 37°C ischemia. NO formation was directly measured by electron paramagnetic resonance (EPR) spectroscopy using the NO trap Fe-MGD (1 mM), while contractile function was measured with a ventricular balloon, and infarct size by TTC staining of heart sections after 45 min of reflow. Preconditioning (PC) increased the recovery of rate pressure product (RPP) by more than two fold with 2.4 fold decrease in infarct size. EPR measurements demonstrated that preconditioning blocked the increase in NO formation during ischemia. When NO formation was supplimented in preconditioned hearts by addition of 20 uM nitrite which was sufficient to restore the NO formation to levels observed in control hearts, the protective effects of preconditioning were abolished. Thus, ischemic preconditioning results in greatly decreased NO formation during subsequent periods of ischemia and this decreased NO formation is associated with the myocardial protection which occurs. Group (n=7) RPP (%PI) Infarct Size (%LV) NO (arb. U) Control 22±4 43±4 61.6±6.1 PC 49±4 18±3 5.3±4.1 PC + NO 19±2 52±6 70±6.3.

Original languageEnglish (US)
JournalFASEB Journal
Issue number5
StatePublished - Mar 20 1998

ASJC Scopus subject areas

  • Agricultural and Biological Sciences (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology


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