Verheij M, Dewit L G, Boomgaard M N, Brinkman H J, van Mourik J A
Department of Radiotherapy, The Netherlands Cancer Institute (Antoni van Leeuwenhoek Huis, Amsterdam.
Radiat Res. 1994 Feb;137(2):202-7.
The effect of radiation on the secretion of von Willebrand factor by endothelial cells was studied in a three-compartment culture system. The release of von Willebrand factor was significantly increased at 48 h after a single gamma-radiation dose of 20 Gy in both the luminal and abluminal direction by 23 (P < 0.05) and 41% (P < 0.02), respectively. To establish whether the enhanced production of von Willebrand factor affected the thrombogenicity of the extracellular matrix, platelet adhesion to the matrix produced by a monolayer of cultured endothelial cells during 48 h after irradiation was analyzed in a perfusion chamber at high shear rate (1300 s-1). Platelet adhesion was significantly increased by irradiation both in the presence and in the absence of plasmatic von Willebrand factor by 65 (P < 0.05) and 34.5% (P < 0.005), respectively. Incubation of the perfusate with a monoclonal antibody that blocks the binding of von Willebrand factor to platelet GPIb (CLB-RAg 35) resulted in an almost complete inhibition of platelet adhesion. These data indicate that radiation enhances platelet adhesion to the the extracellular matrix by an increase in the release of von Willebrand factor by endothelial cells. This event may be important in early radiation-induced vascular pathology.
在三室培养系统中研究了辐射对内皮细胞分泌血管性血友病因子的影响。单次给予20 Gy的γ辐射剂量后48小时，管腔和管腔外方向的血管性血友病因子释放量分别显著增加了23%（P<0.05）和41%（P<0.02）。为了确定血管性血友病因子产量的增加是否影响细胞外基质的血栓形成性，在高剪切速率（1300 s-1）的灌注室中分析了照射后48小时内培养的单层内皮细胞产生的基质上的血小板黏附情况。无论有无血浆血管性血友病因子，照射均使血小板黏附显著增加，分别增加了65%（P<0.05）和34.5%（P<0.005）。用阻断血管性血友病因子与血小板糖蛋白Ib结合的单克隆抗体（CLB-RAg 35）孵育灌注液，几乎完全抑制了血小板黏附。这些数据表明，辐射通过增加内皮细胞释放血管性血友病因子来增强血小板与细胞外基质的黏附。这一事件可能在早期辐射诱导的血管病变中起重要作用。
