Regular alcohol consumption mimics cardiac preconditioning by protecting against ischemia-reperfusion injury

Abstract

Epidemiologic studies indicate that long-term alcohol consumption decreases the incidence of coronary disease and may improve outcome after myocardial infarction. Attenuation of ischemia-reperfusion injury after myocardial infarction improves survival. This study investigates the possibility that alcohol consumption can improve survival after myocardial infarction by reducing ischemia-reperfusion injury. Hearts were isolated from guinea pigs after drinking ethanol for 3-12 weeks and subjected to global ischemia and reperfusion. Hearts from animals drinking ethanol showed improved functional recovery and decreased myocyte damage when compared with controls. Adenosine A1 receptor blockade abolished the protection provided by ethanol consumption. These findings indicate that long-term alcohol consumption reduces myocardial ischemia-reperfusion injury and that adenosine A1 receptors are required for this protective effect of ethanol. This cardioprotective effect of long-term alcohol consumption mimics preconditioning and may, in part, account for the beneficial effect of moderate drinking on cardiac health.

Figure 1

Chronic exposure to ethanol improves recovery of LV-developed pressure during postischemic reperfusion via adenosine A₁ receptors. LV-developed pressure was measured during reperfusion after global ischemia in four groups of isolated guinea pig hearts (n = 10 for each group) following 6 weeks of 10% ethanol consumption (○), in age-matched controls (▵), following 6 weeks of ethanol consumption in the presence of the adenosine A₁ receptor antagonist (DPCPX) (•), and in age-matched controls in the presence of DPCPX (▪). Recovery of LV-developed pressure is significantly greater in hearts from ethanol-treated guinea pigs at each time point measured (P < 0.05). Adenosine A₁ receptor blockade completely abolished ethanol-induced cardioprotection. Data are mean ± SEM. Error bars are not included for open triangles but are less then SEM of closed symbols.

Figure 2

Chronic exposure to ethanol reduces CK release during postischemic reperfusion. CK (units/ml per heart gram-dry-weight) was measured in the coronary effluent during 3-min intervals of postischemic reperfusion from hearts isolated from ethanol-treated guinea pigs as described in Fig. 1 (shaded bars) and controls (open bars). Release of creatine was significantly less from hearts of ethanol-treated animals compared with controls during all 3-min collection periods (P < 0.05). Adenosine A₁ receptor blockade by DPCPX completely abolished the protective effect of ethanol consumption on myocyte injury. Data are presented as mean ± SEM.