HYPOXIA-INDUCED VONWILLEBRAND-FACTOR RELEASE IS BLOCKED BY VERAPAMIL

被引：0

作者：

WILKIE, ME ^{[1
]}

STEVENS, CR ^{[1
]}

CUNNINGHAM, J ^{[1
]}

BLAKE, D ^{[1
]}

机构：

[1] UNIV LONDON LONDON HOSP,COLL MED,ARC BONE & JOINT RES UNIT,LONDON INFLAMMAT GRP,LONDON E1 2AD,ENGLAND

来源：

MINERAL AND ELECTROLYTE METABOLISM | 1992年 / 18卷 / 2-5期

关键词：

CALCIUM ANTAGONIST; ENDOTHELIAL CELLS; HYPOXIA; VERAPAMIL; VONWILLEBRAND FACTOR;

D O I：

暂无

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Hypoxia-induced stimulation of the rate of von Willebrand factor (vWF) release from human umbilical vein endothelial cells in culture, and the influence of the calcium antagonist verapamil, was studied using a system in which a pO2 of 20 mm Hg was achieved over 60 min. The mean +/- SEM rate of vWF release over 60 min in normoxia was 0.42 +/- 0.07% pooled plasma standard. The addition of verapamil did not alter the basal rate of vWF release, but after 60 min of hypoxia, the rate was increased to 0.71 +/- 0.03% plasma standard (p < 0.01). Verapamil at a concentration of 0.1 mug/ml of media had no influence on the stimulated rate of release (0.78 +/- 0.07%), but increasing concentrations of verapamil up to a maximum of 1 mug/ml attenuated the hypoxia induced stimulation (0.48 +/- 0.07%; p = 0.04 vs. hypoxic control). Thus, verapamil at this concentration completely blocked the hypoxia-induced stimulation.

引用

页码：141 / 144

页数：4

共 19 条

[1] VASCULAR DAMAGE AND FACTOR-VIII-RELATED ANTIGEN IN THE RHEUMATIC DISEASES [J].