The Effects of Captopril and Cicaprost on Changes of Cardiac Membrane Fluidity and Lipid Peroxidation  

卡托普利和西卡普鲁斯特对心肌细胞膜流动性及脂质过氧化的保护作用

作　　者：苏志[1] 李元建[1] 陈修[1] 

机构地区：[1]湖南医科大学药理教研室,长沙410078

出　　处：《Journal of Chinese Pharmaceutical Sciences》1993年第2期114-120,共7页中国药学（英文版）

基　　金：Supported by a grant for young researcher from Ministry of Public Health of P.R.C.

摘　　要：The main purpose of this study was to investigate the protective actions of captopril and cicaprost on changes of membrane fluidity of cultured neonatal rat myocardial cells exposed to anoxia and sugar deprivation.Lipid peroxidation level estimated by determining the thiobarbituric acid reactive substance(TBARS)content and lactate dehydrogenase(LDH)released in culture medium was also observed in order to examine other membrane-related changes due to anoxia.Membrane fluidity was monitored by measuring changes in the steady state fluorescence anisotropy(r_s)by fluorescence spectroscopy.The r_s value,TBARS level and LDH release were significantly increased after 3 h anoxia.Captopril(180 μmol/L),cicaprost(30 nmol/L)and indomethacin(1μmol/L)did not alter r_s, TBARS level and LDH activity of normal cultured neonatal rat myocardial cells.However,both captopril and cicaprost significantly prevented the increases of r_s,TBARS content and LDH release in those cells exposed to anoxia and sugar deprivation.lndomethacin abolished the actions of captopril on TBARS production and LDH release,but maintained its membrane fluidity protection.These results indicate that captopril and cicaprost protect membrane fluidity and lipid peroxidation changes in anoxia- injured myocardial cells.The action mechanism of captopril may be due,in part,to stimulation of prostacyclin synthesis and/or release.研究的主要目的旨在探讨卡托普利和西卡普鲁斯特对培养新生乳鼠心肌细胞缺氧缺糖时膜流动性改变的保护作用。为了探讨其它与膜相关的改变,我们同时观察了培养细胞缺氧时脂质过氧化水平及乳酸脱氢酶(LDH)的释放情况。采用荧光分光光度计测定稳态荧光各向异性(r_s)的改变来监测膜流动性,脂质过氧化水平通过测定硫代巴比妥酸反应物(简称 TBARS)含量来评估。实验表明卡托普利(180μmol/L)、西卡普鲁斯特(30 nmol/L)和消炎痛(1μmol/L)对正常新生乳鼠心肌细胞的 r_s 值、TBARS 水平及 LDH 活性均无影响,卡托普利和西卡普鲁斯特均能显著阻止缺氧缺糖所致心肌细胞 r_s 值、TBARS 含量和 LDH 释放的增加,且均有剂量依赖性。消炎痛能取消卡托普利对 TBARS 产生及 LDH 释放的作用,但是仍保留膜流动性的保护作用。这些结果说明卡托普利和西卡普鲁斯特具有保护心肌细胞缺氧损伤时膜流动性和脂质过氧化的作用。卡托普利的保护作用可能是通过促进前列环素的合成和/或释放介导的。

关 键 词：ANOXIA Membrane fluidity Lipid peroxidation CAPTOPRIL Cicaprost Cardiac myocytes 

分 类 号：R972.4[医药卫生—药品]