Endothelial dysfunction and neutrophil adherence as critical events in the development of reperfusion injury.
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.
Lefer
A M
AM
Department of Physiology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA 19107.
Ma
X L
XL
Weyrich
A
A
Lefer
D J
DJ
D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D002415:Cats; D002448:Cell Adhesion / Q000502:physiology; D003331:Coronary Vessels / Q000187:drug effects; D004730:Endothelium, Vascular / Q000503:physiopathology*; D066298:In Vitro Techniques; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology*; D019331:NG-Nitroarginine Methyl Ester; D009504:Neutrophils / Q000502:physiology*; D009569:Nitric Oxide / Q000378:metabolism; D014662:Vasoconstrictor Agents / Q000494:pharmacology
D014662:Vasoconstrictor Agents; D009569:Nitric Oxide; D001120:Arginine; D019331:NG-Nitroarginine Methyl Ester