title: Cardioprotective effect of propranolol from alcohol-induced heart muscle damage as assessed by plasma cardiac troponin-t.
abstract: 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.
authors: Department of Clinical Biochemistry , Guy's, King's and St. Thomas Medical School, King's College London, London, UK.
authors: V B
authors: VB
authors: Patel
authors: R
authors: R
authors: Ajmal
authors: R A
authors: RA
authors: Sherwood
authors: A
authors: A
authors: Sullivan
authors: P J
authors: PJ
authors: Richardson
authors: V R
authors: VR
authors: Preedy
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use*; D000818:Animals; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure; D009202:Cardiomyopathies / Q000139:chemically induced* / Q000503:physiopathology / Q000517:prevention & control*; D004562:Electrocardiography; D000431:Ethanol / Q000008:administration & dosage / Q000009:adverse effects*; D006339:Heart Rate; D007700:Kinetics; D008297:Male; D011433:Propranolol / Q000627:therapeutic use*; D051381:Rats; D017208:Rats, Wistar; D020107:Troponin T / Q000097:blood*
chemical_list: D000319:Adrenergic beta-Antagonists; D015415:Biomarkers; D020107:Troponin T; D000431:Ethanol; D011433:Propranolol