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去氨加压素对正常个体及血管性血友病患者血管性血友病因子抗原II血浆水平的影响。

The effect of DDAVP on plasma levels of von Willebrand antigen II in normal individuals and patients with von Willebrand's disease.

作者信息

McCarroll D R, Ruggeri Z M, Montgomery R R

出版信息

Blood. 1984 Mar;63(3):532-5.

PMID:6607754
Abstract

The infusion of 1-deamino-(8-D-arginine)-vasopressin (DDAVP) causes not only an elevation in factor VIII-related antigen (FVIIIR:Ag), but also a marked elevation of plasma von Willebrand antigen II (vWAgII). vWAgII reaches a peak concentration at 60 min and is elevated 3-8-fold over basal levels in normal individuals and individuals with type I, IIA, and IIB von Willebrand's disease. As the mechanism of hemostatic alteration brought about by DDAVP might be due to release of endothelial cell proteins, endothelial cell cultures were performed. The cultures demonstrated synthesis and secretion of vWAgII, as evidenced by the incorporation of 35S-methionine into the vWAgII molecule. Thus, vWAgII, like FVIIIR:Ag, is an endothelial cell protein.

摘要

输注1-去氨基-(8-D-精氨酸)-血管加压素(DDAVP)不仅会导致VIII因子相关抗原(FVIIIR:Ag)升高,还会使血浆血管性血友病因子抗原II(vWAgII)显著升高。vWAgII在60分钟时达到峰值浓度,在正常个体以及I型、IIA型和IIB型血管性血友病患者中,其浓度比基础水平升高3至8倍。由于DDAVP引起止血改变的机制可能是内皮细胞蛋白的释放,因此进行了内皮细胞培养。培养结果显示vWAgII的合成与分泌,35S-甲硫氨酸掺入vWAgII分子即证明了这一点。因此,vWAgII与FVIIIR:Ag一样,是一种内皮细胞蛋白。

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