Pretreatment with propranolol reduced the increase in plasma cardiac troponin-T induced by acute alcohol administration (75 mmol/kg) in male Wistar rats.
Does propranolol pretreatment reduce acute alcohol-induced myocardial damage as assessed by plasma cardiac troponin-T in male Wistar rats?
Propranolol reduces acute alcohol-induced myocardial damage in rats, suggesting a role for beta-1 and/or beta-2 adrenergic activation in ethanol-induced cardiac lesions.
BACKGROUND: Heavy alcohol consumption from either long-term misuse or binge drinking is associated with poor cardiac contractility, mitochondrial dysfunction, 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 mmol/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 (an inhibitor of acetaldehyde dehydrogenase), various beta-blockers, xanthine oxidase inhibitors, or lisinopril before acute alcohol dosing. In chronic studies, rats were fed alcohol (as 35% of total dietary calories) for 6 weeks. RESULTS: The results of the time course study showed that acute alcohol administration 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 troponin-T were potentiated with cyanamide pretreatment. Acute ethanol, alone or with cyanamide pretreatment, decreased systolic blood pressure and increased heart rates. Beta-blocker pretreatment with propranolol reduced the alcohol-induced increase in plasma troponin-T, whereas lisinopril potentiated this effect. The beta-blockers, atenolol and metoprolol, and the xanthine oxidase 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 rat 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 characterized by raised plasma cardiac troponin-T possibly due to beta1 and/or beta2 adrenergic activation.
Patel et al. (Fri,) conducted a other in Alcohol-induced heart muscle damage. Propranolol vs. Alcohol alone (acute) or control pair-fed rats (chronic) was evaluated on Plasma cardiac troponin-T. Pretreatment with propranolol reduced the increase in plasma cardiac troponin-T induced by acute alcohol administration (75 mmol/kg) in male Wistar rats.
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