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对容量超负荷大鼠模型，用电镜细胞化学方法观察了卡托普利不同时期干预对心肌线粒体膜磷脂结构损伤性改变的作用。结果发现在容量超负荷不同阶段，心肌线粒体皆表现有增生及线粒体嵴膜磷脂结构有程度不等的脱失等损伤性改变。于超负荷后随即卡托普利干预者，心肌线粒体膜磷脂结构改变与对照组比较变化不大（Ｐ＞０．０５），心室作功能力却进一步降低；于造瘘后１月干预者，反映心脏代谢状态的心肌线粒体膜磷脂结构损伤性改变有所减轻，同时部分心室作功参数也有所改善。提示在容量超负荷心脏过早应用转换酶抑制剂不利于心脏重建，而于造瘘后一月干预，可改善心肌代谢和心室功能。
To investigate the effect of captopril on the structural damage of myocardial mitochondrial membrane phospholipid in the capacity-overload rat model by electron microscopy cytochemistry. The results showed that at different stages of capacity overload, myocardial mitochondria showed proliferative and mitochondrial cristae phospholipid structure with varying degrees of loss and other damage. Immediately after captopril intervention, structural changes of mitochondrial membrane phospholipid in myocardial mitochondrial membrane changed little (P> 0.05), and the function of ventricle was further reduced. In January after fistula intervention, Myocardial mitochondrial membrane phospholipid structural damage, which reflects the metabolic state of the heart, has been alleviated. At the same time, some of the ventricular work parameters have also been improved. It is suggested that premature use of ACE inhibitors in capacity overload heart is not conducive to cardiac remodeling, while intervention in January after fistula may improve myocardial metabolism and ventricular function.