福辛普利对阿霉素中毒心肌的保护作用  

The Protective Effects of Fosinopril Against the Adriamycin Toxic induced Myocardium

作　　者：章敏[1] 吕宝经[1] 荣烨之[1] 张亚臣[1] 黄国芳[1] 杨瑾文[1] 

机构地区：[1]上海第二医科大学新华医院心内科,上海200092

出　　处：《上海第二医科大学学报》2002年第1期19-21,38,共4页Acta Universitatis Medicinalis Secondae Shanghai

摘　　要：目的探讨阿霉素对心肌损伤的机制及福辛普利的防治作用。　方法采用大鼠慢性阿霉素中毒模型 ,并随机分为对照组、模型组与福辛普利组。测定心肌钙含量 ,心肌SRCa2 + -ATP酶活性、心肌ATⅡ和脂质过氧化指标。　结果阿霉素可促使心肌脂质过氧化损伤 ,抑制心肌SRCa2 + -ATP酶活性 ,并激活心肌局部RAS ,使ATⅡ生成增多 ,从而导致细胞内钙超负荷 ;福辛普利可拮抗上述途径介导的阿霉素心肌损伤。　结论阿霉素对心肌毒害的机制与脂质过氧化损伤和细胞内钙超负荷有关 ;福辛普利能抗脂质过氧化损伤及提高心肌SRCa2 + -ATP酶活性 ,对防治阿霉素诱导的心肌损伤有一定作用。Objective The toxity of adriamycin on the myocardium and the protective effect of fosinopril on the injured myocardium in rats were studied in this paper. Methods A rat model of chronic adriamycin-induced cardiomyopathy was established and all rats were divided into three groups:control group,adriamycin group and fosinopril+adriamycin group. The content of intramyocardial Ca 2+ ,the activity of sarcoplasm reticulum(SR)Ca 2+ -ATPase and the content of intramyocardial AT Ⅱ were determined. The parameters of lipid peroxidation damage were also measured. Results Adrimycin could cause lipid peroxidation damage, inhibit SR Ca 2+ - ATPase activity and activate cardiac RAS,which resulted in a higher content of AT Ⅱ and intracellular Ca 2+ overloading. Fosinopril could ameliorate the above-mentioned adriamycin-induced myocardial damage. Conclusion The toxicity of adriamycin on the myocardium was related to lipid peroxidation damage and intracellular Ca 2+ overloading. Fosinopril could reduce lipid peroxidation damage and protect SR Ca 2+ -ATPase. Thus it could be effective in the prevention and treatment of adriamycin-induced toxic injury.

关 键 词：肌浆网 CA^2+-ATP酶 钙超负荷 血管紧张素Ⅱ 阿霉素心肌病 福辛普利 

分 类 号：R542.2[医药卫生—心血管疾病]