Long-term inhibition of myocardialinfarction by postconditioning during reperfusion

James Mykytenko, Faraz Kerendi, James Reeves, Hajime Kin, Amanda Zatta, Rong Jiang, Robert Guyton, Jakob Vinten-Johansen, Zhi-Qing Zhao

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78 Citations (Scopus)


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 (30A?3 vs. 39A?2* ) by TTC staining, superoxide anion generation from the post-ischemic coronary arteries by lucigenin-enhanced chemiluminescence [(89A?5 vs. 236A?27* relative light units (RLU/mg)], and neutrophil (PMN) accumulation by immunohistochemical staining in the AAR (52A?11 vs. 84A?14* cells/mm2 myocardium) significantly increased between 3 and 24 h of reperfusion. Postconditioning reduced infarct size (15A?4a? and 27A?3.6a? ), superoxide anion generation (24A?4a? and 43A?11a? RLU/mg), and PMN accumulation (19A?6a? and 45A?8a? cells/mm2 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
Original languageEnglish
Pages (from-to)90 - 100
Number of pages11
JournalBasic Research in Cardiology
Issue number1
Publication statusPublished - 2007

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