Protective and anti-protective effects of acute ethanol exposure in myocardial ischemia/reperfusion

Epidemiological data suggest that a cardioprotective effect of acute alcohol exposure exists in humans. Recent studies in animal models indicate that transient alcohol exposure can indeed reduce myocardial infarct size and exert a preconditioning-like protective effect akin to ischemic preconditioning (IPC). Moreover, the mechanism of alcohol-induced cardioprotection in part resembles the signaling cascade triggered by ischemic preconditioning, with adenosine receptors, PKC, protein tyrosine kinases, and mitochondrial K(ATP) channels all being implicated as key components. However, it was also seen, at least in the rabbit, that if alcohol were present during the ischemic insult, it could block its own protection. The primary protective effect of alcohol use is probably in the chronic setting where alcohol exposure causes a second window type of protection that persists for many days thereafter. Regular moderate drinking should keep the heart in a second window state indefinitely.