关键词: 缺氧, 膜流动性, 脂质过氧化, 卡托普利, 西卡普鲁斯特, 心肌细胞

Abstract: 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 (rs) by fluorescence spectroscopy. The rs value, TBARS level and LDH release were significantly increased after 3 h anoxia. Captopril (180 μmol/L), cicaprost (30 nmol/L) and indomethacin (1 μmol/L) did not alter rs, TBARS level and LDH activity of normal cultured neonatal rat myocardial cells. However, both captopril and cicaprost significantly prevented the increases of rs, TBARS content and LDH release in those cells exposed to anoxia and sugar deprivation. Indomethacin 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.

Key words: Anoxia, Membrane fluidity, Lipid peroxidation, Captopril, Cicaprost, Cardiac myocytes