Endothelial dysfunction and neutrophil adherence as critical events in the development of reperfusion injury

Agents Actions Suppl. 1993:41:127-35.

Abstract

We measured changes in basal release of nitric oxide (NO) and its effect on polymorphonuclear neutrophil (PMN) adherence to endothelial cells (EC) in a feline model of myocardial ischemia and reperfusion (MI/R). Significant reductions in basal NO release occurred 10 minutes following reperfusion, whereas increases in PMN adherence occurred at 20 minutes post-reperfusion. Addition of hSOD blocked the post-reperfusion adherence of PMNs to the endothelium. These results indicate that decreased basal release of NO, following MI/R precedes enhanced PMN adherence to the coronary endothelium, which may lead to PMN-induced myocardial injury.

MeSH terms

  • Animals
  • Arginine / analogs & derivatives
  • Arginine / pharmacology
  • Cats
  • Cell Adhesion / physiology
  • Coronary Vessels / drug effects
  • Endothelium, Vascular / physiopathology*
  • In Vitro Techniques
  • Myocardial Reperfusion Injury / physiopathology*
  • NG-Nitroarginine Methyl Ester
  • Neutrophils / physiology*
  • Nitric Oxide / metabolism
  • Vasoconstrictor Agents / pharmacology

Substances

  • Vasoconstrictor Agents
  • Nitric Oxide
  • Arginine
  • NG-Nitroarginine Methyl Ester