title: Protective effects of aspirin from cardiac hypertrophy and oxidative stress in cardiomyopathic hamsters.
abstract: OBJECTIVE
  To evaluate the capacity of chronic ASA therapy to prevent cardiac alterations and increased oxidative stress in cardiomyopathic hamsters.
  
  
  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 (O(2)(-)) production. At the age of 150 days, the ventricular weight over body weight ratio, resting heart rate, and cardiovascular O(2)(-) 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 O(2)(-) 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.
authors: Department of Pharmacology, Faculty of Medicine, Université de Montréal, Montpetit, QC, Canada.
authors: Rong
authors: R
authors: Wu
authors: David
authors: D
authors: Yin
authors: Nataliya
authors: N
authors: Sadekova
authors: Christian F
authors: CF
authors: Deschepper
authors: Jacques
authors: J
authors: de Champlain
authors: Helene
authors: H
authors: Girouard
mesh_terms: D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D001241:Aspirin / Q000494:pharmacology / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D006332:Cardiomegaly / Q000150:complications* / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D009202:Cardiomyopathies / Q000150:complications* / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D002316:Cardiotonic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D006224:Cricetinae; D005355:Fibrosis; D006339:Heart Rate / Q000187:drug effects; D006352:Heart Ventricles / Q000187:drug effects / Q000473:pathology; D008297:Male; D009206:Myocardium / Q000201:enzymology / Q000473:pathology; D019255:NADPH Oxidases / Q000378:metabolism; D009861:Onium Compounds / Q000494:pharmacology; D009929:Organ Size / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects; D013481:Superoxides / Q000378:metabolism; D013997:Time Factors
chemical_list: D002316:Cardiotonic Agents; D009861:Onium Compounds; D013481:Superoxides; C007517:diphenyleneiodonium; D019255:NADPH Oxidases; C060505:neutrophil cytosolic factor 1; D001241:Aspirin