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[脑血栓形成患者慢性期的抗血小板治疗——评估其对凝血和纤溶参数的影响]

[Antiplatelet therapy in patients with cerebral thrombosis at the chronic phase--assessment of its effect on coagulation and fibrinolytic parameters].

作者信息

Kohriyama T, Tanaka E, Katayama S, Yamamura Y, Nakamura S

机构信息

Third Department of Internal Medicine, Hiroshima University School of Medicine.

出版信息

Rinsho Shinkeigaku. 1994 Aug;34(8):771-6.

PMID:7994982
Abstract

We studied the effect of antiplatelet therapy not only on the secondary prevention of stroke but also on the suppression of vascular damages in patients with cerebral thrombosis at the chronic phase. We measured von Willebrand factor (vWF) as a marker for the endothelial system, and coagulation and fibrinolytic parameters in addition to platelet functions. The platelet aggregation and markers for platelet activation were monitored for the adequate inhibition of platelets. Twenty-one patients were treated with 200 mg ticlopidine. 9 patients with 100 mg ticlopidine and 60-150 mg acetylsalicylic acid, and 18 patients with 200 mg cilostazol daily. The mean duration of follow up was 8.4 +/- 3.0 months. A patient was attacked by a recurrent stroke, but no fatal vascular events occurred during the period. A significant decrease was observed in the collagen- and ADP-induced platelet aggregation and markers for platelet activation such as platelet factor 4 (PF4) and beta-thromboglobulin (beta TG) by the antiplatelet therapy. In addition, the activities of coagulation factor VIII (FVIII) and vWF, markers for vascular damages, showed a significant decrease. The results suggest that the antiplatelet therapy could ameliorate the vascular damage through the inhibition of platelet function. Moreover, thrombin-antithrombin III complex (TAT) and alpha 2-plasmin inhibitor-plasmin complex (PIC), markers for the activation of coagulation and fibrinolytic systems, decreased significantly, suggesting that the treatment inhibits the activation of coagulation and fibrinolytic systems induced by the platelet activation. The activities of FVIII and vWF decreased significantly when the level of beta TG or that of PF4 lowered sufficiently by the treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

我们研究了抗血小板治疗不仅对中风二级预防的效果,还对慢性期脑血栓形成患者血管损伤的抑制作用。我们检测了血管性血友病因子(vWF)作为内皮系统的标志物,以及除血小板功能外的凝血和纤溶参数。监测血小板聚集和血小板活化标志物以确保血小板得到充分抑制。21例患者接受200mg噻氯匹定治疗。9例患者接受100mg噻氯匹定和60 - 150mg阿司匹林治疗,18例患者每日接受200mg西洛他唑治疗。平均随访时间为8.4±3.0个月。有1例患者发生复发性中风,但在此期间未发生致命性血管事件。抗血小板治疗后,胶原和ADP诱导的血小板聚集以及血小板活化标志物如血小板因子4(PF4)和β-血小板球蛋白(βTG)显著降低。此外,血管损伤标志物凝血因子VIII(FVIII)和vWF的活性也显著降低。结果表明,抗血小板治疗可通过抑制血小板功能改善血管损伤。此外,凝血和纤溶系统激活标志物凝血酶 - 抗凝血酶III复合物(TAT)和α2 - 纤溶酶抑制剂 - 纤溶酶复合物(PIC)显著降低,表明该治疗可抑制由血小板活化诱导的凝血和纤溶系统激活。当治疗使βTG或PF4水平充分降低时,FVIII和vWF的活性显著降低。(摘要截短至250字)

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