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Am J Physiol Heart Circ Physiol (February 14, 2002). doi:10.1152/ajpheart.01064.2001
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Articles in PresS, published online ahead of print February 14, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.01064.2001
Submitted on December 5, 2001
Accepted on February 11, 2002

Ketamine abolishes ischemic preconditioning through inhibition of ATP-sensitive K+ channels in rabbit hearts

Jin Han1*, Nari Kim1, Hyun Joo2, and Euiyong Kim1

1 Department of Physiology & Biophysics, College of Medicine, Inje University, Busan, Korea
2 Department of Molecular Science & Technology/Life Science, Ajou University, Suwon, Korea

* To whom correspondence should be addressed. E-mail: phyhanj{at}ijnc.inje.ac.kr.

Although ketamine inhibits KATP channels in rat ventricular myocytes and abolishes the cardioprotective effect of ischemic preconditioning in isolated rat hearts and in rabbits in in vivo, no studies to date specifically address the precise mechanism of this prevention of ischemic preconditioning by ketamine. This study investigated the mechanism of the blockade of ischemic preconditioning by ketamine in rabbit ventricular myocytes using patch-clamp techniques and in rabbit heart slices model for simulated ischemia and preconditioning. In cell-attached and inside-out patches, ketamine inhibited KATP channel activities in a concentration-dependent manner. Ketamine decreased the burst duration and increased the inter-burst duration without a change in the single-channel conductance. In the heart slice model of preconditioning, heart slices preconditioned with a single 5-min anoxia, pinacidil, or diazoxide followed by 15-min reoxygenation were protected against subsequent 30-min anoxia and 1-h reoxygenation, and the cardioprotection was blocked by the concomitant presence of ketamine. These data are consistent with notion that inhibition of sarcolemmal or mitochondrial KATP channels may contribute, at least in part, to the mechanism of the blockade of ischemic preconditioning by ketamine.




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