摘要
２０例急性心肌梗死患者在溶栓后随机分为穿心莲有效成分（ＡＰＩ０１３４，ＡＰＩ）组与对照组，治疗１５ｄ，均同时给予阿司匹林等药物。检测溶栓前后血浆α颗粒膜蛋白（ＧＭＰ－１４０）浓度和ＡＤＰ诱导的血小板聚集反应。结果表明，ＡＰＩ组溶栓后７２ｈ血浆ＧＭＰ－１４０浓度轻度增加，对照组显著性增加（Ｐ＜０．０１）。ＡＰＩ组ＧＭＰ－１４０在溶栓后７２ｈ和１５ｄ均低于对照组，差异有显著意义（均为Ｐ＜０．０５）。ＡＰＩ组１ｍｉｎ和５ｍｉｎ血小板聚集率均低于对照组，差异均有显著意义（７２ｈ，Ｐ＜０．０５；１５ｄ，Ｐ＜０．０１）。研究表明，ＡＰＩ与阿司匹林联合应用可抑制溶栓后血小板的活化，优于阿司匹林单独应用，因此ＡＰＩ有可能用于临床预防溶栓后的再闭塞。
In order to investigate the inhibitive effects of API0134(API) on activation of platelets after thrombolytic therapy, 20 acute myocardiac infarction patients after thrombolytic treatment with urokinase were randomly divided into two groupstreated group with API and control group(n=10 in each group) API was given orally for 15 days,2 groupswere all given Aspirin and other conservative agentsPlasma membrane glycoprotein140(GMP140), and ADPinduced aggregation rate of platelets were observedbefore and after thrombolytic treatmentIn comparison with prethrombolytic treatment status,the concentration of GMP140 72 h after API treatment was only slightly increased, whereas in control group markedly increased(P<001)Comparison between two groups showed the concentration of GMP140 in treated group 72 h as well as 15 days after thrombolytic treatment was significantly lower than in control group (P<005)With regard to the rate of platelets aggregation the treated group showed significant lower value in the 1st and second phase than control group(P<005 after 72 h, P<001 after 15 days) This result showed that API combined with Aspirin may inhibit the activation of platelets after thrombolytic therapy,which was superior than by using Aspirin aloneThus API might prevent from reocclusion after thrombolysis clinically
出处
《同济医科大学学报》
CSCD
1999年第3期230-231,234,共3页
Acta Universitatis Medicinae Tongji
基金
国家自然科学基金
关键词
穿心莲
心肌梗塞
Α颗粒膜蛋白
血小板聚集
API0134
myocardiac infarction
membrane glycoprotein140
thrombolysis
platelet aggregation
