title: Coronary artery endothelial function after myocardial ischemia and reperfusion.
abstract: BACKGROUND
  The consequences of ischemia-reperfusion injury on myocytes has been studied intensely, and previous investigations of methods of myocardial protection during global and regional ischemia have focused on resultant alterations in myocardial function. However, the coronary artery endothelium is also vulnerable to damage, and only recently have investigators been able to assess coronary endothelial function.
  
  
  METHODS
  This review examines some aspects of coronary flow abnormalities that occur after ischemia and reperfusion. In addition, we summarize recent data that address the hypothesis that injury to the coronary artery endothelium may contribute to the pathophysiology of global (and regional) cardiac ischemia and reperfusion.
  
  
  RESULTS
  It appears that ischemia and reperfusion selectively injure a component in the receptor/G-protein complex linking receptor-stimulus coupling to the activation of nitric oxide synthase. Further, oxygen radicals may contribute to this injury. Recent investigations demonstrate that oxygen radicals impair the receptor/G-protein complex specific to the nitric oxide signal transduction pathway rather than causing global receptor/G-protein dysfunction.
  
  
  CONCLUSIONS
  The understanding of endothelial cell function and the elucidation of the nitric oxide pathway should further clarify our understanding of the pathogenesis of endothelial reperfusion injury and coronary vasospasm and contribute to the development of effective therapeutic interventions.
authors.affiliation: Mayo Clinic, Rochester, Minnesota 55905, USA.
authors.forename: J F
authors.initials: JF
authors.lastname: Seccombe
authors.forename: H V
authors.initials: HV
authors.lastname: Schaff
mesh_terms: D000594:Amino Acid Oxidoreductases / Q000502:physiology; D000818:Animals; D003326:Coronary Circulation; D003329:Coronary Vasospasm / Q000503:physiopathology; D003331:Coronary Vessels / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D019204:GTP-Binding Proteins / Q000502:physiology; D017202:Myocardial Ischemia / Q000503:physiopathology*; D015425:Myocardial Reperfusion; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology; D009569:Nitric Oxide / Q000502:physiology; D019001:Nitric Oxide Synthase; D017382:Reactive Oxygen Species / Q000494:pharmacology; D018000:Receptors, Peptide / Q000502:physiology; D015398:Signal Transduction
chemical_list: D017382:Reactive Oxygen Species; D018000:Receptors, Peptide; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D000594:Amino Acid Oxidoreductases; D019204:GTP-Binding Proteins