大鼠心肌缺血再灌时血小板5-HT_(2A)受体变化及腹蛇抗栓酶对心肌的保护作用  

Changes of Platelet 5-HT2A Receptor in Ischemic/Reperfusive Rat and Protection of SVATE on Myocadium

作　　者：庞懿[1] 许澍淮[1] 斯琴 杨丽明 薛全福[1] 

机构地区：[1]中国医学科学院中国协和医科大学基础医学研究所病理生理研究室

出　　处：《基础医学与临床》1998年第2期38-42,37,共6页Basic and Clinical Medicine

基　　金：国家自然科学基金

摘　　要：本文观察了大鼠心肌缺血再灌注后血小板５－ＨＴ２Ａ受体、血浆５－ＨＴ，心肌ＣＰＫ的变化，及蛇毒抗栓酶对其影响。结果显示心肌缺血再灌后，血小板５－ＨＴ２Ａ受体Ｂｍａｘ和Ｋｄ及心肌ＣＰＫ明显减少，血浆５－ＨＴ明显升高。ＳＶＡＴＥ能逆转血小板５－ＨＴ２Ａ受体Ｂｍａｘ、Ｋｄ以及心肌ＣＰＫ变化，但使血浆５－ＨＴ水平进一步升高。正常血小板在体外和２０μｍｏｌ／Ｌ５－ＨＴ温育后，５－ＨＴ２Ａ受体特异结合增加，在此基础上丙给同样剂量５－ＨＴ或与４０ｕｍｏｌ／Ｌ５－ＨＴ温育后５－ＨＴ２Ａ受体特异结合反而下降，ＳＶＡＴＥ同样能逆转受体特异结合的变化。据此，讨论了５－ＨＴ２Ａ受体变化与缺血再灌损伤关系及ＳＶＡＴＥ的保护机理。The changes of platelet 5-HT 2A receptor ,plasma 5-HT level and myocardial CPK activity and the effect of snake venom anti-thrombus enzyme (SVATE ) were observed in the rat subjected to left coronary artery occlusion for one hour followed by one hour reperfusion. The re- sults showed that platelet membrane 5-HT2A receptor binding (using tritiated Ketanserin ) Bmax 、 Kd values and myocardial CPK activity decreased significantly (P<0. 01 , 0. 0l and 0. 001 ,respectively) ,but plasma 5-HT level increased significantly (P<0. 05). SVATE could inverse the changes of 5-HT2A receptor binding Bmax ,Kd and myocardial CPK activity , but incfease plasma 5-HT level. In vitro , the 5-HT 2A receptor binding sites increased after platelet incubation with 20u mol/L 5-HT , but decreased when stimulated with 20 mol/L 5- HT twice or 40 mol/L 5-HT once. SVATE could prevent 20 mol/L 5-HT-induced platelet 5-HT 2A receptor increase. The paradoxical regulation of 5-HT 2A receptor by SVATE proba- bly is due to its blocking or disturbing effect on binding between 5-HT and 5-HT2A receptor rather than inhibition of 5-HT release ,however ,it could further stimulate platelet to release 5-HT . The protective effect of SVATE on ischemic/reperfusive myocardium damage is related to its regulation on platelet 5-HT2A receptor.

关 键 词：心肌缺血 再灌注 血小板 5-HT2A受体 腹蛇抗栓酶 

分 类 号：R542.2[医药卫生—心血管疾病]