title: Long-term inhibition of myocardial infarction by postconditioning during reperfusion.
abstract: Cardioprotection with postconditioning has been well demonstrated after a short period of reperfusion. This study tested the hypothesis that postconditioning reduces infarct size, vascular dysfunction, and neutrophil accumulation after a long-term reperfusion. Canines undergoing 60 min left anterior descending artery (LAD) occlusion were divided into two control groups of either 3 h or 24 h of full reperfusion and two postconditioning groups with three 30 s cycles of reperfusion and re-occlusion applied at the onset of either 3 h or 24 h of reperfusion. Size of the area at risk (AAR) and collateral blood flow during ischemia were similar among groups. In controls, infarct size as percentage of the AAR (30 +/- 3 vs. 39 +/- 2* %) by TTC staining, superoxide anion generation from the post-ischemic coronary arteries by lucigenin-enhanced chemiluminescence [(89 +/- 5 vs. 236 +/- 27* relative light units (RLU/mg)], and neutrophil (PMN) accumulation by immunohistochemical staining in the AAR (52 +/- 11 vs. 84 +/- 14* cells/mm(2) myocardium) significantly increased between 3 and 24 h of reperfusion. Postconditioning reduced infarct size (15 +/- 4 and 27 +/- 3.6 %), superoxide anion generation (24 +/- 4 and 43 +/- 11 RLU/mg), and PMN accumulation (19 +/- 6 and 45 +/- 8 cells/mm(2) myocardium) in the 3 and 24 h reperfusion groups relative to time-matched controls. These data suggest that myocardial injury increases with duration of reperfusion; reduction in infarct size and attenuation in inflammatory responses with postconditioning persist after a prolonged reperfusion. * p < 0.05 24 vs. 3 h control; p < 0.05 postconditioning vs. time-matched control.
authors.affiliation: Cardiothoracic Research Laboratory, Carlyle Fraser Heart Center/ Crawford Long Hospital Emory University School of Medicine, 550 Peachtree Street NE, Atlanta, GA 30308-2225, USA.
authors.forename: James
authors.initials: J
authors.lastname: Mykytenko
authors.forename: Faraz
authors.initials: F
authors.lastname: Kerendi
authors.forename: James G
authors.initials: JG
authors.lastname: Reeves
authors.forename: Hajime
authors.initials: H
authors.lastname: Kin
authors.forename: Amanda J
authors.initials: AJ
authors.lastname: Zatta
authors.forename: Rong
authors.initials: R
authors.lastname: Jiang
authors.forename: Robert A
authors.initials: RA
authors.lastname: Guyton
authors.forename: Jakob
authors.initials: J
authors.lastname: Vinten-Johansen
authors.forename: Zhi-Qing
authors.initials: ZQ
authors.lastname: Zhao
mesh_terms: D000818:Animals; D003097:Collateral Circulation / Q000502:physiology; D003326:Coronary Circulation / Q000502:physiology; D003331:Coronary Vessels / Q000378:metabolism; D003402:Creatine Kinase / Q000097:blood; D004285:Dogs; D004730:Endothelium, Vascular / Q000378:metabolism; D005260:Female; D006321:Heart / Q000503:physiopathology*; D006339:Heart Rate / Q000502:physiology; D008297:Male; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D015425:Myocardial Reperfusion / Q000009:adverse effects / Q000379:methods*; D015428:Myocardial Reperfusion Injury / Q000209:etiology / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D009504:Neutrophils / Q000502:physiology; D013481:Superoxides / Q000378:metabolism; D017725:Ventricular Pressure / Q000502:physiology
chemical_list: D013481:Superoxides; D003402:Creatine Kinase