Mechanisms of myocardial protection produced by chronic ethanol consumption

Recent evidence suggests that chronic ingestion of small quantities of ethanol may protect myocardium from ischemic injury by activating many of the endogenous signal transduction elements that have been implicated during other forms of preconditioning. Studies conducted in a variety of animal models in vitro and in vivo have indicated that chronic ethanol consumption improves functional recovery after global ischemia, reduces biochemical markers of ischemic injury, and decreases myocardial infarct size. Many of these beneficial actions appear to occur independent of alterations in systemic and coronary hemodynamics and transmural myocardial perfusion. To date, adenosine type 1 (A(1)) receptors, alpha(1)-adrenoceptors, the epsilon isoform of protein kinase C (PKC), and adenosine triphosphate-dependent potassium (K(ATP)) channels have been shown to mediate cardioprotection associated with chronic ethanol ingestion. These data suggest another mechanism by which chronic, intermittent consumption of ethanol may reduce overall cardiovascular mortality, decrease the incidence of coronary artery disease, and improve survival after myocardial infarction in humans. In this brief review, we discuss current evidence supporting a role for endogenous signaling in chronic ethanol-induced myocardial protection against ischemic injury.