摘要
用离体大鼠心脏氧反常模型研究阿魏酸钠（ＳＦ）对氧反常心肌功能，代谢及结构的影响。缺氧４０ｍｉｎ后复氧１０ｍｉｎ，ＳＦ０．２１、０．４２、０．８５、１．６９ｍｍｏｌ．Ｌ－１可显著减少心肌复氧时的肌酸磷酸激酶（ＣＰＫ）的释放及脂质过氧化产物雨二醛（ＭＤＡ）的生成，明显提高心肌谷胱苷肽过氧化物酶（ＧＳＨ－ＰＸ）和超氧化物歧化酶（ＳＯＤ）活力。ＳＦ１．６９ｍｍｏｌ．Ｌ－１明显减轻心肌超微结构的损害。缺氧３０ｍｉｎ后复氧２０ｍｉｎ，ＳＦ０．４２ｍｍｏｌ．Ｌ－１明显增加冠脉流量，促进心肌功能的恢复，明显降低心肌钙含量。结果提示ＳＦ的保护氧反常心肌作用可能与其抗氧自由基毒性作用，减轻脂质过氧化反应及钙超载有关。Ｐ＜０．０１图１核及核周结构正常，肌原纤维排列规则、整齐，肌节结构清晰，∑Ｍ×６０００图２ 线粒体嵴模糊、紊乱、稀疏，肌原纤维结构紊乱．∑Ｍ×８３００图３ 线粒体嵴紊乱、消失，部分溶解为空泡状．肌原纤维结构紊乱，∑Ｍ×１００００图４ 核周间隙不增宽，肌节结构清晰，线粒体嵴较清晰．∑Ｍ×８３００明显下降．３～５ｍｉｎ时有所回升．５ｍｉｎ后随着缺氧时间延长ＣＦ明显下降．再恢复供氧后有所回升．但与正常组比较，Ｐ＜０．０１?
Effect of sodium ferulate (SF) on myocardium structure, function and metabolism during oxygen paradox were studied in the isolated perfused hearts Of rat. During reoxygenation 10 min after hypoxia 40 min. SF 0. 21, 0. 42, 0. 85, 1. 69 mmol·L-1 significantly decreased the release of myocardium creatine phosphokinase (CPK) and the production of toxic lipid peroxide malondialdehyde (MDA), increased the activity of myocardium eroxide dismutase (SOD) and reduced damage of ultrastructure of myocardial cell. In the isolated rat hearts with reoxygenation 20 minafter hypoxia 30 min, SF 0. 42 mmol·L-1significantly increased the coronary flow, improved the recovery of cardiac function and attenuated myocardial Ca2+ accumulation. This favorable effect may be due to its protection against the toxic effects of antioxygen free radicals and lipid peroxidation, and due to its prevention from Ca2+accumulation in myocardium.
出处
《中国药理学通报》
CAS
CSCD
北大核心
1995年第1期24-28,共5页
Chinese Pharmacological Bulletin
关键词
阿魏酸钠
氧自由基
心肌缺血
再灌注损伤
保护
sodium ferulate
oxygenparadox
oxygen-derived free radicals
lipidperoxidation
