Department of Pharmacology, Faculty of Medicine, Université de Montréal, Montpetit, QC, Canada.
Oxid Med Cell Longev. 2012;2012:761710. doi: 10.1155/2012/761710. Epub 2012 Jul 4.
To evaluate the capacity of chronic ASA therapy to prevent cardiac alterations and increased oxidative stress in cardiomyopathic hamsters.
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.
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.
评估慢性阿司匹林治疗预防心肌病仓鼠心脏改变和氧化应激增加的能力。
雄性叙利亚心肌病和同窝对照仓鼠从 60 天大开始口服接受阿司匹林。动物在 150、250 和 350 天处死，以评估心脏肥大和心血管组织超氧阴离子（O(2)(-)）产生的时间过程。在 150 天，心肌病仓鼠的心室重量与体重比、静息心率和心血管 O(2)(-)产生明显高于对照组。在 250 天，除了这些参数随年龄的持续恶化外，血压开始下降并出现心力衰竭迹象。在这些心肌病仓鼠中，慢性阿司匹林治疗（a）完全预防了升高的 O(2)(-)产生和 NAD(P)H 氧化酶活性，（b）显著减缓了心脏肥大和纤维化的发展。
慢性阿司匹林治疗可显著预防心肌病仓鼠心脏功能和结构的恶化以及氧化应激的增加。我们的发现表明阿司匹林具有预防心脏功能障碍的治疗潜力。
