摘要
目的:观察急性心肌梗死(AMI)和稳定型心绞痛(SAP)血液中血小板表面糖蛋白GPⅡb和GPⅢa的动态变化,探讨急性心肌缺血前、后血小板的活性。方法:61例住院的心病患者,其中AMI32例,SAP29例,采用竞争性酶联免疫方法比较AMI及SAP患者发病后24h,第2天、第3天、1财2周时血中血汀反GPⅡb和GPⅢa的含量动态变化,并进行统计学分析。
To observe dynamic changes of platelet membrane glucoprotein(GP) Ⅱb and GPⅢa in blood circulation in acute myocardial infarction(AMI)and stable angina pectoris(SAP)of coronary heart disease, in order to investigate platelet activation before and after acute iechemic onset. Methods: Platelet membrane GPⅡb and GPⅢa were examined for 6lh os- pitalized cases with AMI or SAP at 24 hours, second day, third day,first week and second week after the attacks,using EIA and statistical analyses. Results:Platelet GPⅡb and GPⅢa contents of SAP group at 24 h, second day, third day, 1st,2nd week[6.86 ± 2.74/5 .94 ± 1 .96,6.25 ± 1 .85/5 .61 ± 1 .45,6.74 ± 2.67/6.07 ± 1 .99,5 .96 ± 2.35/5 .76 ± 1 .59,7.56 ± 2.72/7. 17 ± 2.45 (× 10~4 /Pt respectively)]were higher than those of control group[3 .91 ± 0.36/4 .53 ±0.51 (× 10~4 / Pt) ],there was significant between-group difference, it showed that platelets were activated. GPⅡb and GPⅢa of AMI group at 24 h, second, third day, lst, 2nd week[8.38 2.38/7.62 ± 1 .69, 8.39 ± 2.55/7.64 ± 1 .86, 8.32 ± 2 .38/ 7.29 ± 1 .45,7.40 ± 2. 10/6.73 ± 1 .46, 6.53 ± 2. 18/6.36 ± 1 .29(x 10~4 /Pt)]were higher than the control group(P< 0. 01 ), there was significant between-group difference. GPⅡb and GPⅢa of AMI group had peak time at least within 3 days and a negative correlation with time. Comparison of GPⅡb and GPⅢa of AMI group with SAP group in first 3 days showed significant differences,but there were no significant differences between these tow groups at lst weed and 2nd week. Con- clusions:Platelets activation at AMI persisted 3 days peak time at least, it showed that GPⅡb and GPⅢa took part in the attack of AMI. So it is necessary to use the platelet GPⅡb and GPⅢa inhibitor in AMI, especially within first 3 days.
出处
《天津医药》
CAS
1999年第11期646-648,共3页
Tianjin Medical Journal
关键词
心肌梗塞
心绞痛
血小板
膜糖蛋白类
血小板活化
myocardial infarction acute disease angina pectoris blood platelets membrane glycoproteins plate- let activation