Abstract
The cardioprotective effects of YM934, an ATP-sensitive potassium channel opener (KCO), on isolated canine cardiomyocytes were examined. Exposure of isolated canine cardiomyocytes to YM934 (10 μM) resulted in an increase of potassium channel opening activity in whole cell patch clamp technique. Glibenclamide (1 μM) reversed the channel opening activity induced by YM934. Pretreatment of the cardiomyocytes with YM934 caused a potent inhibition KCL (20 mM)-induced increase in [Ca2+]i. Cromakalim also inhibited the KCL-induced increase in [Ca2+]i under the same experimental conditions. The ratio of alive to dead cells and the release of creatine kinase from isolated cardiomyocytes during a 120-min hypoxia / 15-min reoxygenation period were dose-dependently (YM934; 0.1–10 μM) attenuated; 71–93% of the preischemic value for the ratio of alive/dead cells and 76–58% of the nontreated hearts for the release of creatine kinase. These results suggest that YM934 has a direct cardioprotective effect against ischemia/reperfusion injury of canine cardiac myocytes, possibly through opening ATP-sensitive potassium channels. Drug Dev. Res. 48:113–120, 1999. © 1999 Wiley-Liss, Inc.
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