Abstract
Cardiac postconditioning is elicited by brief episodes of ischemia (or other pharmacologic mimetics including volatile anesthetics) just prior to and during the first minutes of reperfusion. Caveolin-3 (Cav-3), has been extensively studied for its role in cardiac protection induced by preconditioning stimuli. Cav-3 is a scaffolding protein that provides a platform to organize many proteins including survival kinases. Whether Cav-3 is important to postconditioning is unclear. Littermate controls (LC) and Cav-3 knockout (Cav-3 KO) mice underwent 30 min of LAD occlusion, with and without 5 min isoflurane exposure (1.4%) immediately after index ischemia, followed by 2 hr reperfusion and determination of infarct size. Isoflurane produced a potent postconditioning effect in LC mice. Isoflurane-induced postconditioning was abrograted in Cav-3 KO mice. Such data indicate that as with preconditioning, Cav-3 and caveolae localized signaling is critical to anesthetic induced postconditioning.
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