Moderate alcohol consumption induces sustained cardiac protection by activating PKC- and Akt

Zhou, Hui-Zhong, Joel S. Karliner, and Mary O. Gray. Moderate alcohol consumption induces sustained cardiac protection by activating PKCand Akt. Am J Physiol Heart Circ Physiol 283: H165–H174, 2002. First published February 28, 2002; 10.1152/ajpheart.00408.2001.—C57BL/6 mice were fed 18% ethanol (vol/vol) in drinking water for 12 wk. Isovolumic hearts were subjected to 20 min of ischemia and 30 min of reperfusion on a Langendorff apparatus. There were no differences in baseline hemodynamic function between hearts from ethanol (EtOH)-fed mice and controls. However, prior alcohol consumption doubled recovery of left ventricular developed pressure (68 8 vs. 33 8 mmHg for controls; n 10, P 0.05) and reduced creatine kinase release by half (0.26 0.04 vs. 0.51 0.08 U min 1 g wet wt 1 for controls; n 10, P 0.05). EtOH feeding doubled expression of activated protein kinase C epsilon (PKC) (n 6, P 0.05); whereas PKC inhibition blocked protection during ischemia-reperfusion. EtOH feeding also increased expression of Akt threeto fivefold (n 6, P 0.05), whereas PKC inhibition prevented increases in Akt kinase activity. We conclude that signaling pathways involving PKCare critical for sustained EtOH-mediated cardioprotection and that Akt may be a downstream effector of resistance to myocardial reperfusion injury.