Wilkie M E, Stevens C R, Cunningham J, Blake D
Department of Nephrology, Royal London Hospital, UK.
Miner Electrolyte Metab. 1992;18(2-5):141-4.
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 microgram/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 microgram/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.
采用一种在60分钟内使氧分压达到20毫米汞柱的系统,研究了缺氧对培养的人脐静脉内皮细胞中血管性血友病因子(vWF)释放速率的刺激作用,以及钙拮抗剂维拉帕米的影响。在常氧条件下,60分钟内vWF释放的平均±标准误速率为0.42±0.07%混合血浆标准。加入维拉帕米并未改变vWF释放的基础速率,但在缺氧60分钟后,速率增加至0.71±0.03%血浆标准(p<0.01)。培养基中浓度为0.1微克/毫升的维拉帕米对刺激释放速率无影响(0.78±0.07%),但维拉帕米浓度增加至最高1微克/毫升时,可减弱缺氧诱导的刺激作用(0.48±0.07%;与缺氧对照组相比,p=0.04)。因此,该浓度的维拉帕米完全阻断了缺氧诱导的刺激作用。