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及机制。方法腹主动脉部分缩窄法制作急性压力超负荷模型。50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、心肌碱性成纤维细胞生长因子(bFGF)蛋白表达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 ,随后bFGF蛋白表达也升高 ;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 ,延迟bFGF蛋白表达 ,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。结论小剂量卡托普利能有效防治急性压力超负荷引起的大鼠心肌损伤 。
Objective To evaluate effect and mechanism of captopril on the prevention of myocardial injury induced by acute pressure overload in rats.Methods Acute pressure overloads were made by ligating abdominal aorta in50male rats,and the rats were divided into three groups:15rats as operated group,20rats as lowdose of captopril treated group,and15rats as sham-operated group.Sham-operated group was served as control.Each captoˉpril treated rat was delivered by direct gastric gavage in a dose of30mg·kg -1 ·d -1 .At different time points after surgery,myocardial mechanics,metabolic enzyme(lactate dehydrogenase and succinate dehydrogenase)activity,the content of myocardial angiotensinⅡand bFGF protein were measured,and pathologic analysis was done in each group.Results Hypoxia injury including mitochondria swelling was obvious,activity of succinate dehydrogenase and±dp/dt max ÷LVSP of left ventricle were decreased significantly,and the content of myocardial angiotensinⅡwas elevated markedly after acute pressure overload.However,after the elevation of AngⅡ,content of bFGF protein elevated markedly at first and then fell to control levels.Compared with operation group,hypoxia injury and deˉcreased activity of succinate dehydrogenase were inhibited,±dp/dt max ÷LVSP were improved significantly and the rise of bFGF protein was alleviated in treated group.Conclusions Hypoxia injury of rats after acute pressure overˉload can be prevented effectively with low dose of catopril,AngⅡand bFGF may play an important role in the mechanism.
出处
《中国微循环》
2004年第4期221-224,共4页
Journal of Chinese Microcirculation
基金
国家自然科学基金资助 (No.39600041)
