Chien K R, Crie J S, Decker R S, Wildenthal K
Cardiovasc Res. 1983 Jul;17(7):407-14. doi: 10.1093/cvr/17.7.407.
Ligation of the circumflex artery of anaesthetised, open-chest rabbits caused a progressive increase in nonsedimentable cathepsin D activity in severely ischaemic myocardium and an anatomical redistribution of the enzyme from lysosomes into the cytosol, along with progressive ultrastructural signs of cellular damage and necrosis. Chlorpromazine pretreatment (15 mg X kg-1 intravenously) reduced the increase in nonsedimentable cathepsin D activity slightly, but no appreciable protective effect on the anatomical redistribution of the enzyme or the development of ultrastructural signs of necrosis could be detected. It is concluded that in this experimental model of myocardial infarction, high concentrations of chlorpromazine have a mild stabilising action on lysosomes, but the drug has minimal if any effect in protecting the heart from ischaemic damage.
结扎麻醉开胸兔的冠状动脉旋支，会使严重缺血心肌中不可沉淀的组织蛋白酶D活性逐渐升高，该酶从溶酶体向胞质溶胶发生解剖学上的重新分布，同时伴有细胞损伤和坏死的渐进性超微结构特征。氯丙嗪预处理（静脉注射15mg/kg）可略微降低不可沉淀的组织蛋白酶D活性的升高，但未检测到对该酶解剖学重新分布或坏死超微结构特征发展的明显保护作用。得出的结论是，在这个心肌梗死实验模型中，高浓度氯丙嗪对溶酶体有轻度稳定作用，但该药物对保护心脏免受缺血性损伤的作用微乎其微（如果有作用的话）。
