中文摘要：

目的：研究急性缺氧对大鼠远端肺静脉平滑肌细胞（PVSMC）细胞内钙浓度（[Ca^2＋]i）的影响及L型电压依赖性钙通道（VDCC）阻断剂硝苯地平的作用，为缺氧性肺动脉高压发病机制的进一步研究提供理论依据。方法：胶原酶消化法培养大鼠远端PVSMC，利用荧光显微镜和细胞内钙浓度检测系统观测急性缺氧（4％O2）、高钾（60mmol／LKCl）溶液对PVSMC的[Ca^2＋]i影响及硝苯地平的干预作用。结果：对照组PVSMC的[Ca^2＋]i随时间变化维持基线水平；缺氧组PVSMC急性缺氧后，[Ca^2＋]i迅速升高并维持平台水平，△[Ca^2＋]i达82．83nmol／L＋23．03nmol／L；硝苯地平干预组PVSMC予急性缺氧和5μmol／L硝苯地平干预后，[Ca^2＋]i升高幅度较小；高钾溶液孵育PVSMC后，[Ca^2＋]i迅速增高，5μmol／L硝苯地平能完全阻断PVSMC的[Ca^2＋]i对高钾溶液的反应。结论：急性缺氧可使大鼠远端PVSMC的[Ca^2＋]i升高，其机制可能与激活PVSMC的VDCC和另外的非VDCC依赖的钙通道导致细胞外Ca^2＋内流有关。

英文摘要：

Objective： To study the effect of acute hypoxia on intracellular calcium cation concentration （[Ca^2＋]i） in rat distal pulmonary venous smooth muscle cells （PVSMC） and the role of the L-type voltage-dependent Ca^2＋ channels （VDCC） antagonist nifedipine. Methods： The rat distal PVSMC were cultured by collagenase digestion. The effects of acute hypoxia （4% 02 ） and high KC1 （60 mmol/L） on [Ca^2＋]i in PVSMC and the role of nifedipine were tested by fluorescence microscopy and InCyte [Ca^2＋ ]i measurement system. Results： The time course of [Ca^2＋ ]i in control PVSMC was stable at baseline. Acute hypoxia induced a marked increase in [Ca^2＋ ]i in PVSMC that rose quickly to a peak of/k [Ca^2＋ ]i =82.83＋23.03 nmol/L and followed by a plateau. 5μmol/L nifedipine partially attenuated the [Ca^2＋ ]i response to acute hypoxia and the peak of/k [Ca^2＋ ]i averaged 42.17±6.18 nmol/L in PVSMC. 60 mmol/L KC1 caused a quick increase in [Ca^2＋ ]i in PVSMC with the peak of/k [Ca^2＋ ]i = 183. 03 ~ 37. 84 nmol/L and 5 μmol/L nifedipine completely blocked the [-Ca^2＋ ]i response to KC1 in PVSMC. Conclusion： Acute hypoxia increased the [Ca^2＋ ]i in rat distal PVSMC. An increase in [Ca^2＋]μ induced by acute hypoxia may the related to the influx of Ca^2＋ through VDCC and another VDCC-independent Ca^2＋ channels in PVSMC.