title: Acute endothelial reperfusion injury after coronary artery bypass grafting.
abstract: Coronary artery endothelium exhibits functional impairment after ischemia and reperfusion. Canine left anterior descending coronary arteries were exposed to ischemia (60 minutes) followed by reperfusion (60 minutes) through a left internal mammary artery graft. In organ chamber experiments, control (left circumflex coronary artery) and reperfused (left anterior descending coronary artery) arterial segments were contracted with prostaglandin F2 alpha and exposed to hypoxia (oxygen tension = 35 +/- 5 mm Hg). Reperfused coronary rings with endothelium exhibited contractions to hypoxia that were significantly greater than contractions in control rings with endothelium (+78% +/- 8% and +14% +/- 5%, respectively; p < 0.05). This phenomenon could be blocked by NG-monomethyl-L-arginine. Electron microscopic studies showed platelet adhesion and aggregation, denudation of the endothelium and disruption of the intercellular junctions, edematous subendothelial matrix, and vesiculation of the smooth muscle cells in reperfused LAD. Swelling, vacuole formation, and loss of neurofilament occurred in the nerve fibers accompanying the vessels. These phenomena were not observed in control vessels. This study demonstrates that early after coronary artery bypass grafting, hypoxia can induce coronary vasospasm mediated by an L-arginine-dependent metabolic pathway in the endothelium. The ultrastructural changes in the coronary endothelium include platelet adhesion, aggregation, and platelet-induced contraction of coronary smooth muscle. The endothelium-dependent hypoxic coronary vasospasm and ultrastructural changes in the coronary endothelium may play an important role in the pathogenesis of myocardial ischemia and infarction after coronary artery bypass grafting.
authors.affiliation: Division of Thoracic and Cardiovascular Surgery, Chang Gung Memorial Hospital, Chang Gung Medical College, Taipei, Taiwan, Republic of China.
authors.forename: P J
authors.initials: PJ
authors.lastname: Lin
authors.forename: C H
authors.initials: CH
authors.lastname: Chang
authors.forename: Y S
authors.initials: YS
authors.lastname: Lee
authors.forename: Y Y
authors.initials: YY
authors.lastname: Chou
authors.forename: J J
authors.initials: JJ
authors.lastname: Chu
authors.forename: J P
authors.initials: JP
authors.lastname: Chang
authors.forename: M J
authors.initials: MJ
authors.lastname: Hsieh
mesh_terms: D000208:Acute Disease; D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D015687:Cell Hypoxia / Q000187:drug effects; D001026:Coronary Artery Bypass / Q000009:adverse effects*; D003331:Coronary Vessels / Q000187:drug effects / Q000473:pathology*; D015237:Dinoprost / Q000494:pharmacology; D004285:Dogs; D004730:Endothelium, Vascular / Q000187:drug effects / Q000473:pathology*; D005260:Female; D008297:Male; D008855:Microscopy, Electron, Scanning; D017348:Microscopy, Electron, Scanning Transmission; D008954:Models, Biological; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000473:pathology* / Q000503:physiopathology; D009200:Myocardial Contraction / Q000187:drug effects; D009204:Myocardial Revascularization; D009569:Nitric Oxide / Q000037:antagonists & inhibitors; D010973:Platelet Adhesiveness / Q000187:drug effects; D010974:Platelet Aggregation / Q000187:drug effects*; D015427:Reperfusion Injury / Q000209:etiology / Q000473:pathology*; D019323:omega-N-Methylarginine
chemical_list: D019323:omega-N-Methylarginine; D009569:Nitric Oxide; D001120:Arginine; D015237:Dinoprost