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and Akt
Cardiology Section, San Francisco Veterans Affairs Medical Center and Department of Medicine and Cardiovascular Research Institute, University of California, San Francisco, California 94143
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
wt1 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 three- to fivefold (n = 6, P < 0.05), whereas PKC inhibition prevented increases in Akt kinase activity. We conclude that signaling pathways involving PKC- are critical for sustained EtOH-mediated cardioprotection and
that Akt may be a downstream effector of resistance to myocardial reperfusion injury.
heart; ischemia; reperfusion; ethanol; signaling
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