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4℃下通过凝固作用破坏瑞斯托菌素辅因子。

Destruction of ristocetin cofactor by coagulation at 4 degrees C.

作者信息

Lloyd J V, Tunbridge L J, Rodgers S E, Hondow J A, Russell W J

出版信息

Thromb Res. 1985 Mar 15;37(6):659-68. doi: 10.1016/0049-3848(85)90195-1.

DOI:10.1016/0049-3848(85)90195-1
PMID:3922085
Abstract

Ristocetin cofactor (VIIIR:RCo) and factor VIII-related antigen (VIIIR:Ag) were measured in anticoagulated and non-anticoagulated blood incubated at 4 degrees C, room temperature (RT) or 37 degrees C for 24 hours. A marked decrease in VIIIR:RCo, to almost undetectable levels, and a smaller decrease in VIIIR:Ag occurred when whole blood clotted at 4 degrees C. These changes were slight or absent when blood clotted at RT or 37 degrees C. VIIIR:RCo lost at 4 degrees C was not recoverable by further incubation at 37 degrees C but the less-marked loss of VIIIR:Ag was partially recovered. In blood which had clotted at 4 degrees C there was a change in the electrophoretic profile of VIIIR:Ag on crossed immunoelectrophoresis: there was more anodal migration of the VIIIR:Ag peak, consistent with a decrease in the mean molecular size. Further experiments showed that the decrease in VIIIR:RCo during coagulation at 4 degrees C preceded the decrease in fibrinogen levels. In cell-free plasma VIIIR:RCo also decreased markedly when coagulation occurred at 4 degrees C. The results show that loss of VIIIR:RCo occurs when blood is allowed to clot at 4 degrees C: this is not due to cryoprecipitation and does not require the presence of blood cells. The data suggest that it is probably caused by plasma proteases activated early in the coagulation pathway.

摘要

在4℃、室温(RT)或37℃下孵育24小时的抗凝和非抗凝血中测量瑞斯托菌素辅因子(VIIIR:RCo)和因子VIII相关抗原(VIIIR:Ag)。当全血在4℃凝结时,VIIIR:RCo显著下降至几乎检测不到的水平,VIIIR:Ag下降幅度较小。当血液在RT或37℃凝结时,这些变化轻微或不存在。在4℃损失的VIIIR:RCo在37℃进一步孵育后无法恢复,但VIIIR:Ag损失较小的部分得以恢复。在4℃凝结的血液中,VIIIR:Ag在交叉免疫电泳中的电泳图谱发生了变化:VIIIR:Ag峰有更多的阳极迁移,这与平均分子大小的减小一致。进一步的实验表明,在4℃凝血过程中VIIIR:RCo的下降先于纤维蛋白原水平的下降。在无细胞血浆中,当在4℃发生凝血时,VIIIR:RCo也显著下降。结果表明,当血液在4℃凝结时会发生VIIIR:RCo的损失:这不是由于冷沉淀,也不需要血细胞的存在。数据表明,这可能是由凝血途径早期激活的血浆蛋白酶引起的。

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