Nitric oxide and the vascular endothelium in myocardial ischemia-reperfusion injury

Ann N Y Acad Sci. 1999 Jun 30;874:354-70. doi: 10.1111/j.1749-6632.1999.tb09251.x.


The normal coronary vascular endothelium (VE) tonically releases nitric oxide (NO) by converting L-arginine to citrulline by a constitutive NO synthase. Reperfusion after myocardial ischemia reduces basal and stimulated release of NO. This "vascular reperfusion injury" is mediated largely by neutrophils (PMN) through specific interactions between adhesion molecules on the endothelium and the PMN, an interaction that precedes myocyte injury. NO inhibits the PMN-mediated reperfusion injury by direct effects on both the PMN and the vascular endothelium. Cardioprotective strategies include augmentation of endogenous NO by the precursor L-arginine and the administration of exogenous NO donors at the time of perfusion, which (1) attenuates PMN adherence to the coronary artery and venous endothelium, (2) reduces PMN-mediated endothelial dysfunction, (3) reduces PMN accumulation in the area at risk, and (4) reduces infarct size. Hence, NO represents a powerful therapeutic tool with which to attenuate the consequences of ischemia-reperfusion injury on vascular injury and infarction.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Cell Adhesion Molecules / physiology
  • Coronary Vessels / metabolism
  • Endothelium, Vascular / metabolism
  • Endothelium, Vascular / physiopathology*
  • Myocardial Ischemia / metabolism
  • Myocardial Ischemia / physiopathology*
  • Myocardial Reperfusion Injury / physiopathology*
  • Nitric Oxide / metabolism
  • Nitric Oxide / physiology*


  • Cell Adhesion Molecules
  • Nitric Oxide