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Am J Physiol Heart Circ Physiol (February 28, 2002). doi:10.1152/ajpheart.00408.2001
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Articles in PresS, published online ahead of print February 28, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00408.2001
Submitted on May 17, 2001
Accepted on February 20, 2002

Moderate alcohol consumption induces sustained cardiac protection by activating {epsilon} protein kinase C and Akt

Hui-Zhong Zhou1, Joel S Karliner1, and Mary O Gray1*

1 Cardiology Section, San Francisco Veterans Affairs Medical Center, San Francisco, California, USA; Department of Medicine, University of California, San Francisco, San Francisco, California, USA

* To whom correspondence should be addressed. E-mail: gray{at}medicine.ucsf.edu.

C57BL/6 mice were fed 18% ethanol (vol/vol) in drinking water for 12 weeks. Isovolumic hearts were subjected to 20 min ischemia and 30 min reperfusion on a Langendorff apparatus. There were no differences in baseline hemodynamic function between hearts from ethanol-fed mice and controls. However, prior alcohol consumption doubled recovery of LV developed pressure (68 ± 8 vs. 33 ± 8 mm Hg for Controls; n=10, P<0.05) and reduced CK release by half (0.26 ± 0.04 vs. 0.51 ± 0.08 U/min/gww for Controls; n=10, P<0.05). Ethanol feeding doubled expression of activated {epsilon}PKC (n=6, P<0.05); whereas PKC inhibition blocked protection during ischemia-reperfusion. Ethanol feeding also increased expression of Akt three- to five-fold (n=6, P<0.05); whereas PKC inhibition prevented increases in Akt kinase activity. We conclude that signaling pathways involving {epsilon}PKC are critical for sustained ethanol-mediated cardioprotection and that Akt may be a downstream effector of resistance to myocardial reperfusion injury.




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