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1 Anatomy, Physiology, and Genetics, Uniformed Services University of the Health Sciences, Bethesda, MD, USA
* To whom correspondence should be addressed. E-mail: lschwartz{at}usuhs.mil.
Transient episodes of ischemic preconditioning (PC) render myocardium protected against subsequent lethal injury following ischemia and reperfusion. Recent studies indicate that application of short, repetitive ischemia only during the onset of reperfusion following the lethal ischemic event may obtain equivalent protection. We assessed whether such ischemic postconditioning (Postcon) is cardioprotective in pigs by limiting lethal injury. Barbital-anesthetized open-chest pigs underwent 30 min complete occlusion of the left anterior descending coronary artery and 3 hr reflow. PC was elicited by two cycles of 5-min occlusion plus 10-min reperfusion before the 30-min occlusion period. Postcon was elicited by three cycles of 30-sec reperfusion, followed by 30-sec re-occlusion, after the 30-min occlusion period and prior to 3-hr reflow. Infarct size (% area-at-risk using triphenyl tetrazolium chloride macrochemistry, means±SE) after 30 min ischemia was 26.5±5.2% (n = 7). PC markedly limited myocardial infarct size (2.8±1.2%, n = 7, p
0.05 vs. controls). However, Postcon had no effect on infarct size (37.8±5.1%, n=7). Within the subendocardium, Postcon increased phosphorylation of Akt (74±12%) and ERK-1/2 (56±10%) compared to control hearts subjected only to 30-min occlusion and 15-min reperfusion (P0.05), and these changes were not different from the response triggered by PC (n=5 each group). Phosphorylation of downstream p70S6K was also equivalent in PC and Postcon groups. These data do not support the hypothesis that application of 30-second cycles of repetitive ischemia during reperfusion exerts a protective effect on hearts subjected to lethal ischemia, but this is not due to a failure to phosphorylate ERK and Akt during early reperfusion.
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