摘要
目的 :探讨小剂量卡托普利防治急性压力超负荷大鼠心肌损伤的作用。方法 :腹主动脉部分缩窄法制作急性压力超负荷模型。 5 0只大鼠随机分为对照组、腹主动脉部分缩窄组和药物干预组。药物干预组给予卡托普利 30mg (kg·d)灌胃。分别测定各组大鼠心肌力学、心肌代谢酶活性、心肌血管紧张素Ⅱ (AngⅡ )含量及心肌超微病理分析。结果 :急性压力超负荷大鼠心肌超微结构出现明显缺氧性损伤 ,琥珀酸脱氢酶活性降低 ,收缩、舒张功能相对下降 ,心肌中AngⅡ含量显著升高。小剂量卡托普利可基本抑制压力超负荷大鼠心肌中AngⅡ的升高 ,显著减轻心肌的形态损伤、代谢酶活性降低和心肌收缩、舒张功能下降。结论
Objective:To evaluate the effect of captopril in the prevention of myocardial injury induced by acute pressure overload in rats.Methods:Acute pressure overloads were made by ligating abdominal aorta in 50 male rats, and the rats were divided into three groups: 15 rats as simple operated group, 20 rats as low dose of captopril treated group,and 15 rats as sham operated group. Sham operated group was served as control. Each captopril treated rat as delivered by direct gastric gavage in a dose of 30 mg·kg -1 ·d -1 . At different time points after sugery, myocardial mechanics and metabolic enzyme(lactate dehydrogenase and succinate dehydrogenase) activity were measured, and pathologic analysis was done in each group.Results:Hypoxia injury including mitochondria swelling was obvious, activity of succinate dehydrogenase and ±dp/dtmax÷LVSP of left ventricle were decreased significantly, but the content of myocardial angiotensin II was elevated markedly after acute pressure overload.Compared with simple operation group, hypoxia injury and decreased activity of succinate dehydrogenase were inhibited and ±dp/dtmax÷LVSP were improved significantly in treated group.Conclusion:Hypoxia injury of rats after acute pressure overload can be prevented effectively with low dose of captopril.
出处
《临床心血管病杂志》
CAS
CSCD
北大核心
2002年第12期638-640,共3页
Journal of Clinical Cardiology
基金
国家自然科学基金资助项目 (No .396 0 0 0 4 1)