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Oxidative Medicine and Cellular Longevity
Volume 2012 (2012), Article ID 761710, 8 pages
Research Article

Protective Effects of Aspirin from Cardiac Hypertrophy and Oxidative Stress in Cardiomyopathic Hamsters

1Department of Pharmacology, Faculty of Medicine, Université de Montréal, Pavillon Roger-Gaudry, 2900 Edouard Montpetit, Montréal QC, Canada H3T 1J4
2Clinical Research Institute of Montreal (CRIM), 110 Pine Ave. West, Montréal QC, Canada H2W 1R7

Received 10 April 2012; Revised 31 May 2012; Accepted 1 June 2012

Academic Editor: Adrian Manea

Copyright © 2012 Rong Wu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Objective. To evaluate the capacity of chronic ASA therapy to prevent cardiac alterations and increased oxidative stress in cardiomyopathic hamsters. Methods and Results. Male Syrian cardiomyopathic and age-matched inbred control hamsters received ASA orally from the age of 60 days. Animals were sacrificed at the age of 150, 250, and 350 days to evaluate the time course of cardiac hypertrophy and cardiovascular tissue superoxide anion ( ) production. At the age of 150 days, the ventricular weight over body weight ratio, resting heart rate, and cardiovascular production were much higher in cardiomyopathic hamsters than those in control. At the age of 250 days, in addition to the continual deterioration of these parameters with age, the blood pressure started to fall and the signs of heart failure appeared. In these cardiomyopathic hamsters, chronic ASA treatment (a) completely prevented elevated production and the NAD(P)H oxidase activity, (b) significantly slowed down the development of the cardiac hypertrophy and fibrosis. Conclusions. Chronic ASA treatment significantly prevents the deterioration of cardiac function and structure as well as the increased oxidative stress in the cardiomyopathic hamster. Our findings suggest that ASA presents a therapeutic potential to prevent cardiac dysfunction.