免疫性血管炎血液高凝状态及药物治疗实验研究

Experimental study of hypercoagulation and effects of drugs on immune vasculitis

目的探讨免疫性血管炎是否存在血液高凝状态、其与血管病变的关系及药物作用的影响。方法建立免疫性血管炎模型,检测外周血小板数量、血小板聚集功能,流式细胞仪检测血小板活性标志Annexin V,ELISA法检测凝血酶原片断F1+2,HE染色、弹力纤维染色及电镜观察血管病理改变。结果免疫性血管炎急性期血小板数量异常增高,为(931.33±254.19)×109/L,与正常对照组(640.67±132.22)×109/L比较,差异有统计学意义。血小板聚集功能和由Annexin V检测的血小板活性标志明显升高,分别为(38.9±13.4)%比(20.9±8.5)%(22.55±6.00)%比(6.31±1.84)%,差异有统计学意义。凝血酶原片断F1+2活性在模型组有明显增高,为(215.93±66.04)pmol/L,与正常对照组(128.22±6.46)pmol/L比较,差异有统计学意义。应用阿司匹林可以明显降低上述各指标,大剂量丙种球蛋白注射(IVIG)不能降低血小板数目和功能,仅能降低凝血酶原片断F1+2活性。但阿司匹林和IVIG对血管炎病理改善的作用相似,差异无统计学意义。结论免疫性血管炎存在血液高凝状态,阿司匹林能改善血液高凝状态,减轻血管炎的病理损害。

Objective To study the hypercoagulation and the effects of drugs on immune vasculitis. Methods The rabbit models of immune vasculitis were reproduced by intravenous injection of bovine serum albumin twice. Peripheral platelet number, platelet aggregation and the population of Annexin V in platelets were detected. Prothrombin fragment F1 ＋ 2 was dectected by ILISA method. The pathological changes of immune vasculifis were analyzed using hematoxylin ＆ eosin staining, elastic fibers staining and electron microscopy. Results The platelet number at the acute phase significantly increased in immune vasculitis model group compared with that in control group,which were （931.33 ± 254. 19） × 10^9/L vs （640. 67 ±132.22） × 10^9/L. The platelet aggregation and the population of Annexin V also significantly increased from （38.9 ± 13.4） % to （20. 9 ±8.5） % and （22. 55 ±6. 00） % to （6. 31 ± 1.84） %. The level of prothrombin fragment F1 ＋ 2 in model group was significantly higher than that in normal group, which was （215.93 ± 66. 04） pmol/L vs （ 128.22 ± 6. 46）pmol/L）. Aspirin treatment could inhibit the number and activity of platelet, and could also inhibit the activity of coagulation, while IVIG could not inhibit the number and activity of platelet. Both drugs could improve the vessels damages of immune vasculitis. Conclusion A hypercoagulation state exists in immune vasculitis, and aspirin can improve the inflammation damage of vessels through inhibiting platelets and coagulation activity.