Cardioprotective Effect of Propranolol From Alcohol-Induced Heart Muscle Damage as Assessed by Plasma Cardiac Troponin-T

  1. Vinood B. Patel,
  2. Raheela Ajmal,
  3. Roy A. Sherwood,
  4. Andrew Sullivan,
  5. Peter J. Richardson,
  6. Victor R. Preedy*

Article first published online: 11 APR 2006

DOI: 10.1111/j.1530-0277.2001.tb02294.x

Issue

Alcoholism: Clinical and Experimental Research

Alcoholism: Clinical and Experimental Research

Volume 25, Issue 6, pages 882–889, June 2001

Additional Information

How to Cite

Patel, V. B., Ajmal, R., Sherwood, R. A., Sullivan, A., Richardson, P. J. and Preedy, V. R. (2001), Cardioprotective Effect of Propranolol From Alcohol-Induced Heart Muscle Damage as Assessed by Plasma Cardiac Troponin-T. Alcoholism: Clinical and Experimental Research, 25: 882–889. doi: 10.1111/j.1530-0277.2001.tb02294.x

Author Information

  1. Departments of Clinical Biochemistry (VBP, RA, RAS) and Cardiology (PJR), Guy's, King's and St. Thomas Medical School, King's College London, London, UK; Safety Pharmacology (AS), Safety Assessment, GlaxoSmithKline, Ware, UK; Department of Nutrition and Dietetics (VRP), King's College London, Franklin-Wilkins Building, London, UK.

*Reprint requests: Dr. Victor R. Preedy, Department of Nutrition and Dietetics, School of Life Sciences, King's College London, Franklin-Wilkins Building, 150 Stamford Street, London, SE1 9NN, UK; Fax: 44-207-848-4185; E-mail: victor.preedy@kcl.ac.uk

Publication History

  1. Issue published online: 11 APR 2006
  2. Article first published online: 11 APR 2006
  3. Received for publication February 28, 2000; accepted March 20, 2001.

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Keywords:

  • Alcoholic Cardiomyopathy;
  • Troponin-T;
  • Heart;
  • Rat;
  • Alcohol

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 β1 and/or β2 adrenergic activation.

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