中文摘要：

本文旨在研究急性缺氧对微动脉血管平滑肌细胞（vascular smooth muscle cells,VSMCs）膜电生理特性的影响。分离出豚鼠小脑前下动脉（anterior inferior cerebellar artery,AICA）段,胶原酶A消化后用显微镊去除微动脉外层结缔组织,然后给予无糖低氧的灌流液,同时应用全细胞膜片钳技术观察VSMCs膜电流的变化。结果显示：（1）当钳制电压在40mV时,急性缺氧引起一个反应幅度为（36.4±9.2）pA的外向电流,细胞静息膜电位从（33.2±1.9）mV超极化到（38.4±1.5）mV。急性缺氧电压依赖性地增强VSMCs外向电流,主要增强0～＋40mV电压区间的激活电流幅度,＋40mV激活电流幅度从（650±113）pA增加到（1900±197）pA。背景灌流K＋通道阻断剂tetraethylammonium（TEA,1mmol/L）后,急性缺氧对VSMCs外向电流的增强作用显著减小。（2）急性缺氧使AICA上VSMCs的细胞膜电阻（R input）从（234±63）MΩ增加到（1211±201）MΩ,细胞膜电容（C input）从（279.3±83.2）pF减少至（25.4±1.9）pF。联合应用30μmol/L非选择性缝隙连接阻断剂18β-甘草次酸（18β-glycyrrhetinic acid,18βGA）和10mmol/L TEA后,急性缺氧对VSMCs外向电流的影响基本消失。以上结果提示,豚鼠AICA急性缺氧可能通过激活VSMCs大电导钙激活钾通道（BK Ca）引起K＋外向电流,舒张血管,从而保障脑部血流供应;同时通过抑制细胞间缝隙连接使急性缺氧造成的伤害限制在局部。

英文摘要：

The aim of the present study was to investigate the effects of acute hypoxia on the electrophysiological properties of vascular smooth muscle cells （VSMCs） in arteriole. Guinea-pig anterior inferior cerebellar artery （A1CA） segments were isolated, and outer layer connective tissue was removed by collagenase A digestion and microforceps. By perfusion with physical saline solution containing no glucose and low oxygen, VSMC model of acute hypoxia was established. The model was studied by whole-cell patch clamp recording technique. Results were shown as below： （1） Acute hypoxia induced an outward current with amplitude of （36.4 ±9.2） pA at holding potential of-40 mV, and the rest potential （RP） of the VSMCs was hyperpolarized from （-33.2 ±1.9） mV to （-38.4 ±1.5） mV. Acute hypoxia increased the outward current of VSMCs in a voltage-dependent manner, this enhancing effect being more pronounced at potentials ranging from 0 to ＋40 mV. The whole-cell membrane current of VSMCs induced by step command （＋40 mV） increased from （650 4- 113） pA to （1 900 -4- 197） pA. In the presence of 1 mmol/L tetraethylammonium （TEA）, the enhancement of the VSMC membrane current by acute hypoxia was significantly reduced. （2） Acute hypoxia increased the membrane resistance （Rinput） of the VSMCs in A1CA from （234 ± 63） MΩ to （1 211 ± 201） MΩ, and decreased the membrane capacitance （Cinput） from （279.3 ± 83.2） pF to （25.4 ±1.9） pF. In the presence of 30 μmol/L 18β-glycyrrhetinic acid （1813GA） and 10 mmol/L TEA, the effects of acute hypoxia on the membrane current of VSMCs were nearly abolished. These results suggest that acute hypoxia causes vascular hyperpolarization and vasodilation, possibly by activating big conductance Ca2＋-activated K＋ channels （BKc,） of the VSMCs, and inhibits gap junctions between VSMCs, thus improving microcirculation and localizing the hypoxia-induced damage.