Cardioprotective effect of propranolol from alcohol-induced heart muscle damage as assessed by plasma cardiac troponin-T

Background: Heavy alcohol consumption from either long-term misuse or binge drinking is associated with poor cardiac contractility, mitochondrial dysf unction, and ventricular arrhythmias. The aim of this study was to measure circulating cardiac troponin-T as a marker for myocardial damage following acute and chronic alcohol administration. Methods: In acute studies, male Wistar rats were treated with alcohol (75 m mol/kg body weight, intraperitoneal) and plasma was collected 2.5 hr after alcohol administration for analysis of rat cardiac troponin-T. In addition, rats were pretreated with cyanamide tan inhibitor of acetaldehyde dehydrog enase), various beta-blockers, xanthine oxidase inhibitors, or lisinopril b efore acute alcohol dosing, In chronic studies, rats were fed alcohol las 3 5% of total dietary calories) for 6 weeks. Results: The results of the time course study showed that acute alcohol adm inistration significantly raised plasma cardiac troponin-T levels after 2.5 hr and 6 hr, but not after 24 hr. The effects of alcohol on cardiac tropon in-T were potentiated with cyanamide pretreatment. Acute ethanol, alone or with cyanamide pretreatment, decreased systolic blood pressure and increase d heart rates. Beta-blocker pretreatment with propranolol reduced the alcoh ol-induced increase in plasma troponin-T, whereas lisinopril potentiated th is effect. The beta-blockers, atenolol and metoprolol, and the xanthine oxi dase inhibitors, allopurinol and oxypurinol, were unable to reduce elevated troponin-T. However, pretreatment with the beta-blocker timolol moderated the acute alcohol-induced increase in troponin-T. In the chronic alcohol ra t model, no differences were observed between alcohol and control pair-fed rats, suggesting the inducement of tolerance. Conclusions: In conditions of acute exposure, ethanol-induced lesions are c haracterized by raised plasma cardiac troponin-T possibly due to beta (1) a nd/or beta (2) adrenergic activation.