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Cardioprotective Effect of Propranolol From Alcohol‐Induced Heart Muscle Damage as Assessed by Plasma Cardiac Troponin‐T
Author(s) -
Patel Vinood B.,
Ajmal Raheela,
Sherwood Roy A.,
Sullivan Andrew,
Richardson Peter J.,
Preedy Victor R.
Publication year - 2001
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.2001.tb02294.x
Subject(s) - medicine , troponin , xanthine oxidase , troponin i , metoprolol , carvedilol , atenolol , propranolol , endocrinology , myocardial infarction , pharmacology , blood pressure , heart failure , chemistry , biochemistry , enzyme
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 β 1 and/or β 2 adrenergic activation.