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Does inhibition of swelling-activated chloride channels with DCPIB abolish the cardioprotective effect of remote ischemic preconditioning dialysate against necrosis in cultured rabbit cardiomyocytes?
Does inhibition of swelling-activated chloride channels with DCPIB abolish the cardioprotective effect of remote ischemic preconditioning dialysate against necrosis in cultured rabbit cardiomyocytes?
Swelling-activated chloride channels are essential for the cardioprotective effects of remote ischemic preconditioning against cardiomyocyte necrosis, likely via interaction with PKCε.
Implicates swelling-activated chloride channels in rIPC cardioprotection in vitro; hypothesis-generating and requires in vivo validation before clinical consideration.
We have previously shown that remote ischemic preconditioning induced in cardiomyocytes by a brief direct incubation in rabbit blood dialysate, originated from other rabbits initially subjected to brief periods of limb ischemia/ reperfusion, given prior exposure to a prolonged ischemia/reperfusion protects cardiomyocytes against necrosis. In this study, we examined the hypothesis that sarcolemmal protein kinase C epsilon interacts with the swellingactivated Cl-channel to both enhance cardiomyocyte volume regulation and protect against cardiomyocyte necrosis in limb ischemia/reperfusion remote ischemic preconditioning.
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Gregory J. Wilson (2014) studied this question.
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