Acute alcohol effects on cardiac pro‐ and anti‐apoptotic pathways in the perfused adult rat heart

Abstract

Cardiovascular disease is among the major causes for increased morbidity and mortality rates. High alcohol consumption may lead to cardiomyopathy, cardiac arrhythmias, and a suite of other disorders (Movva R, Int J Cardiol, 2012). Previous studies in our lab have linked the AKT/PI3K pathway to cardiovascular disease. We also believe increased oxidative stress is a result of high alcohol consumption in cardiovascular disease. In this study we investigate the role of key genes (AKT, super oxide dismutase (SOD‐3), and Caspase‐9) that contribute to cardiac myopathy with acute (30min) alcohol retrograde coronary perfusion of the heart. Our results demonstrate that AKT expression is diminished with acute alcohol exposure which is consistent with the moderate alcohol; however, high alcohol treatment has increased expression over low and moderate alcohol exposure. The Capsase‐9 expression was decreased with high alcohol treatment while low and moderate alcohol had little effect on expression as compared to control. High alcohol treatment diminished SOD‐3 gene expression but low and moderate alcohol treatment had no effect on expression as compared to control. These results suggest that acute high alcohol consumption (e.g., binge drinking) can lead to increased oxidative stress, and malfunction of antioxidant proteins in cardiomyopathy. The data implies that the increased cell death in alcoholic cardiomyopathy may not be dependent on the Bcl‐xL pathway and downstream Caspase‐9. It is important to note that the data was collected from acute studies which may be different with chronic studies.