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出血热的主要病理变化为全身小血管损伤,小血管的变化可能是病毒及其毒素和抗原抗体复合物作用的结果。组织细胞缺氧也是导致内皮细胞损伤的原因。近年来,应用免疫荧光法测定血浆中Ⅷ因子相关抗原,也证实了患者血管内皮细胞受损。本文从测定6-酮前列腺素F_(1α)(PGF_(1α))的能力,探讨血管内皮细胞功能状况及其发病中的作用。 材料 1986年12月~1987年1月,从本院和浙江天台县人民医院,外科手术患者6例、出血热发热期3例、休克期5例(其中重型休克3例),局部取1~1.5cm长的小静脉标本。 方法 取正常入枸橼酸抗凝血,分离出富含血小板血浆(PRP),血小板浓度调节至200×10~9/L后加入50μlTris缓冲液,再加ADP最终浓度达2μm、观察2~3min,作血小板聚集试验(PAgT),为空白对照。后将冷冻的活组织取出,称重,加入一定量4℃ Tris缓冲液、制成2%浸出液,置4℃冰浴,于
The main pathological change of hemorrhagic fever is systemic small vessel injury, which may be the result of the action of the virus and its toxin and antigen-antibody complex. Histological cell hypoxia is also the cause of endothelial cell damage. In recent years, the application of immunofluorescence assay Ⅷ factor-related plasma antigen, but also confirmed the patient’s vascular endothelial cell damage. In this study, we investigated the function of vascular endothelial cells and their role in the pathogenesis of 6-ketoprostaglandin F (1α) (PGF_ (1α)). Materials December 1986 ~ January 1987, from our hospital and Zhejiang Tiantai People’s Hospital, surgical patients in 6 cases, 3 cases of hemorrhagic fever, shock in 5 cases (including 3 cases of severe shock), the local take 1 ~ 1.5cm long venules. Methods Anticoagulation with citric acid was normalized and platelet rich plasma (PRP) was isolated. After the platelet concentration was adjusted to 200 × 10 ~ 9 / L, 50μl Tris buffer was added. The final concentration of ADP was 2μm, and observed for 2 ~ 3min , For platelet aggregation test (PAgT), as a blank control. After frozen living tissue removed, weighed, adding a certain amount of Tris buffer 4 ℃, made of 2% leachate, set 4 ℃ ice bath, at