中文摘要：

目的观察急性缺氧对豚鼠耳蜗螺旋动脉平滑肌细胞电生理特性的影响。方法应用全细胞膜片钳技术观察急性缺氧对微动脉段上平滑肌细胞膜电流、膜电位（RP）、膜电容（Cinput）、膜电导（Ginput）或膜电阻（Rinput）的影响。结果①急性缺氧显著增加平滑肌细胞Rinput降低Ginput和Cinput。Rinput从（4so±88）MΩ增加到（2229±310）Mn（P〈0．01），Cinput从（77．3±8．3）pF减少至（114±0．7）pF（P〈0．01）。48％（15／31）急性缺氧净电流的I／V曲线几乎是线性，翻转电位（-32．6±2.5）mV与细胞静息膜电位（-35．8±4．5）mV十分接近（P〉0．05）。②急性缺氧电压依赖的增强部分平滑肌细胞（16／31）外向电流，主要增强0～＋40mV区间的电流幅度，背景灌流18β-甘草次酸阻断细胞间的缝隙连接后，急性缺氧使0mV激活电流幅度从（27．8±7．5）pA增加到（89．3±12．8）pA（P〈0．01），＋20mV从（88．0±185）pA增加到（211．1±32．5）pA（P〈0．01），＋40mv从（213．9±21．6）pA增加到（448．0±46．5）pA（P〈0．01）。预灌流四乙胺后，急性缺氧对SMA平滑肌细胞外向电流的增强作用显著减弱。结论急性缺氧通过激活SMA平滑肌细胞膜上大电导Ca^2＋激活K＋通道，血管舒张，保证耳蜗循环的血液供应,同时通过抑制SMA平滑肌细胞间缝隙连接使急性缺氧产生的伤害信息局限在局部。

英文摘要：

[ Objective ] To investigate the effects of acute hypoxia on the electrophysiological properties of VSMCs in guinea-pig spiral modiolar artery, [Methods] Whole-cell patch clamp recordings were performed to study the effects of acute hypoxia on the whole-cell membrane current, resting membrane potential （RP）, membrane input capacitance （Cinput）, and membrane input resistance （Rinput, or its reciprocal membrane input conductance, Ginput） of the vascular smooth muscle cell （VSMC） embedded in the arteriolar segment. [Results] Acute hypoxia increased the Rinput of the VSMC in SMA from （480±88） MΩ to （2229±310） MΩ （P〈0.01）, and decreased the Cinput from （77.3±8.3） pF to （11.4±0.7） pF （P〈0.01）. The hypoxia-indueed net current show an approximately linear I/V relation with a reversal potential （-32.6±2.5） mV very close to the resting potential of the recorded cell （-35.8±4.5） mV （P〉0.05）. Acute hypoxia increased the outward current of the VSMC in a voltage-dependent manner, this enhancing effect being more pronounced at potentials ranging from 0 to ＋40 mV. In the presence of 18 β-glyeyrrhetinie acid, the whole-cell membrane current of the VSMC induced by step commands （0, ＋20mV and ＋40mV） was increased from （27.8±7.5） pA to （89.3±12.8） pA （P〈0.01）, （88.0± 18.5） pA to （211.1±32.5） pA （P〈0.01） and （213.9±21.6） pA to （448.0±46.5） pA （P〈0.01） respectively. In the presence of tetraethylammonium, the enhancement of the VSMC membrane current by acute hypoxia was sig- nificantly reduced. [Conclusions] Acute hypoxia causes vascular vasodilation by activating big conductance Ca2＋ - activated K＋ channels of the VSMC, and inhibits gap junctions between VSMCs, thus improving microcirculation and localizing the hypoxia-induced damage.