title: Endothelial dysfunction and neutrophil adherence as critical events in the development of reperfusion injury.
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.
authors.affiliation: Department of Physiology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA 19107.
authors.forename: A M
authors.initials: AM
authors.lastname: Lefer
authors.forename: X L
authors.initials: XL
authors.lastname: Ma
authors.forename: A
authors.initials: A
authors.lastname: Weyrich
authors.forename: D J
authors.initials: DJ
authors.lastname: Lefer
mesh_terms: 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
chemical_list: D014662:Vasoconstrictor Agents; D009569:Nitric Oxide; D001120:Arginine; D019331:NG-Nitroarginine Methyl Ester