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Diacylglycerol delays pHiovershoot after reperfusion and attenuates contracture in isolated, paced myocytes.

Although protein kinase C (PKC) plays a pivotal role in ischemic preconditioning, it is not clear what the end effector is that protects the myocardium. In isolated, paced (1.25 Hz, 36-37°C) adult rat cardiomyocytes, the effects of PKC preactivation by diacylglycerol on cell motion, intracellular Ca2+ concentration ([Ca2+]i; indo 1), and intracellular pH (pHi; seminaphthorhodafluor-1) during simulated ischemia-reperfusion (I/R) were investigated. The degree of reperfusion-induced contracture was significantly attenuated in the myocytes pretreated with 10 μM 1,2-dioctanoyl- sn-glycerol (DOG; n = 19) compared with the untreated myocytes ( n = 23, P < 0.02). There were no differences in twitch amplitude, end-diastolic [Ca2+]i, or peak-systolic [Ca2+]iduring I/R between the DOG-pretreated and untreated myocytes. Although there were no differences in pHiduring ischemia, the pHiovershoot during reperfusion was significantly delayed in the DOG-pretreated myocytes compared with the untreated myocytes ( n = 17 for each, P < 0.01). Chelerythrine completely abolished the favorable effects of DOG on the reperfusion-induced contracture and the pHi overshoot. These data suggest that diacylglycerol attenuates I/R injury in isolated, paced cardiomyocytes, which may be related to the slower pHi overshoot during reperfusion.