Porta M, Ricchetti I, La Selva M, Bertagna A, Molinatti G M
Diabetes Res. 1984 Nov;1(4):219-21.
Plasma von Willebrand factor was studied for quantitative and qualitative assessment in basal conditions and after release from the endothelium, as elicited by venous stasis of the forearm, in 8 healthy subjects and 8 patients with diabetic microangiopathy. von Willebrand factor was measured as factor VIII-related antigen (VIII R:Ag) and ristocetin co-factor (VIII R:Co). Its molecular size distribution was evaluated by bidimensional immunoelectrophoresis. The patients had higher basal levels of VIII R:Ag (171 +/- 45% vs 64 +/- 11% of plasma pooled from 20 healthy donors, p less than 0.05) and VIII R:Co (144 +/- 11% vs 88 +/- 8%, p less than 0.01). After stasis, both moieties increased significantly in the 2 groups, remaining higher in the patients (VIII R:Ag = 292 +/- 74% vs 89 +/- 18%, p = 0.01; VIII R:Co = 216 +/- 25% vs 116 +/- 10%, p less than 0.01). No differences in the molecular size distribution were observed between patients and controls, nor within the 2 groups before and after stasis. It is concluded that, in diabetic microangiopathy, the endothelial cells synthesize and store increased amounts of structurally normal von Willebrand factor.
对8名健康受试者和8名糖尿病微血管病变患者在基础状态下以及在前臂静脉淤滞引发内皮细胞释放后,进行了血管性血友病因子的定量和定性评估。血管性血友病因子作为因子VIII相关抗原(VIII R:Ag)和瑞斯托霉素辅因子(VIII R:Co)进行测量。通过双向免疫电泳评估其分子大小分布。患者的VIII R:Ag基础水平较高(分别为171±45%和64±11%,后者为来自20名健康供体的混合血浆,p<0.05),VIII R:Co也较高(分别为144±11%和88±8%,p<0.01)。淤滞后,两组中这两个部分均显著增加,患者组仍较高(VIII R:Ag=292±74%和89±18%,p=0.01;VIII R:Co=216±25%和116±10%,p<0.01)。患者与对照组之间以及两组在淤滞前后的分子大小分布均未观察到差异。得出结论,在糖尿病微血管病变中,内皮细胞合成并储存了数量增加的结构正常的血管性血友病因子。