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双嘧达莫诱导的冠状动脉闭塞大鼠缺血性坏死的减轻。

Dilazep-induced reduction of ischemic necrosis in rats with coronary artery occlusion.

作者信息

Chiariello M, Brevetti G, Genovese A, Cataffo A, Ambrosio G, Condorelli M

出版信息

Int J Cardiol. 1983;2(3-4):339-48. doi: 10.1016/0167-5273(83)90004-9.

DOI:10.1016/0167-5273(83)90004-9
PMID:6840902
Abstract

To assess whether dilazep reduces myocardial necrosis we assigned 72 rats that survived coronary artery occlusion to 3 groups. The first control group (n = 26) received coronary occlusion and was untreated. The second group (n = 21) received coronary occlusion and was treated with dilazep (150 micrograms/kg s.c.) every 8 hours for 48 hours. The third group (n = 25) was sham-operated. Forty-eight hours later the creatine-kinase activity of the left ventricle was measured. The calculated left ventricular fraction that survived the occlusion was larger in dilazep-treated rats (44.5 +/- 4.1% of left ventricle) than in controls (31.2 +/- 3.2%; P less than 0.05). Twenty-six more rats also underwent coronary occlusion; 12 were controls and the remaining 14 were treated with dilazep at the same time and dose as before and killed 21 days after occlusion. Infarct size was evaluated on histological sections of the hearts by planimetry. The amount of left ventricle preserved from necrosis was larger in dilazep-treated rats, 82.1 +/- 0.9%, compared to controls 69.5 +/- 1.4% (P less than 0.05). Dilazep seems effective in preserving myocardial tissue from ischemic necrosis, and its beneficial effects are long-lasting, producing permanent reduction of infarct size.

摘要

为评估双嘧达莫是否能减少心肌坏死,我们将72只冠状动脉闭塞后存活的大鼠分为3组。第一对照组(n = 26)接受冠状动脉闭塞且未治疗。第二组(n = 21)接受冠状动脉闭塞,并每8小时皮下注射双嘧达莫(150微克/千克),持续48小时。第三组(n = 25)进行假手术。48小时后,测量左心室的肌酸激酶活性。双嘧达莫治疗的大鼠中,计算得出的闭塞后存活的左心室分数(占左心室的44.5±4.1%)高于对照组(31.2±3.2%;P<0.05)。另外26只大鼠也接受冠状动脉闭塞;12只为对照组,其余14只同时接受与之前相同剂量的双嘧达莫治疗,并在闭塞后21天处死。通过平面测量法在心脏组织切片上评估梗死面积。双嘧达莫治疗的大鼠中,未发生坏死的左心室量更大,为82.1±0.9%,而对照组为69.5±1.4%(P<0.05)。双嘧达莫似乎能有效保护心肌组织免受缺血性坏死,且其有益作用持久,能使梗死面积永久性减小。

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Int J Cardiol. 1983;2(3-4):339-48. doi: 10.1016/0167-5273(83)90004-9.
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