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为了从离子通道水平上探讨机体低氧适应的离子机制,本实验将雄性 SD 大鼠随机分为常氧对照组和慢性间歇性低氧组[氧浓度(10 ± 0.5) %, 间断缺氧每天 8 h]。用酶解法急性分离单个大鼠肺内动脉平滑肌细胞(pulmonary artery smoothmuscle cells, PASMCs),以全细胞膜片钳技术记录 PASMCs 膜上的电压门控性钾通道 (voltage-gated potassium channel, KV) 电流,观察急性缺氧对慢性间歇性低氧大鼠 PASMCs 的 KV 的影响, 为机体适应低氧能力提供实验依据。结果显示:⑴常氧对照组在电流钳下,急性缺氧可使膜电位明显去极化(由-47.2 ±2.6 mV 去极到 -26.7 ±1.2 mV ); 在电压钳下, 急性缺氧可显著抑制 KV电流(+60 mV 时, KV电流密度从 153.4 ± 9.5 pA/pF降到 70.1 ± 10.6 pA/pF), 峰电流的抑制率为(57.6 ± 3.3) %, 电流-电压关系曲线向右下移。⑵慢性间歇性低氧组KV电流密度随低氧时间延长而逐渐减少(慢性低氧10 d后就有显著性意义),电流- 电压关系曲线逐渐右下移。⑶急性缺氧对慢性间歇性低氧大鼠PASMCs KV电流的抑制作用随慢性间歇性低氧时间延长而逐渐减弱。上述观察结果提示慢性间歇性低氧减弱急性缺氧对 KV 的抑制, 这可能是机体低氧适应的一种重要机制。
In order to explore the mechanism of hypoxia adaptation from the ion channel level, male SD rats were randomly divided into normoxia control group and chronic intermittent hypoxia group [oxygen concentration (10 ± 0.5)%, intermittent hypoxia everyday 8 h]. Pulmonary artery smooth muscle cells (PASMCs) from a single rat were isolated by enzymatic digestion, and the voltage-gated potassium channel (KV) currents on PASMCs were recorded by whole-cell patch clamp technique. To observe the effect of acute hypoxia on KV of chronic intermittent hypoxic rats PASMCs and provide experimental basis for the body to adapt to hypoxia. The results showed that: (1) Under normoxia in acute normoxia control group, acute hypoxia significantly depolarized membrane potential (from -47.2 ± 2.6 mV to -26.7 ± 1.2 mV); under voltage clamp, acute hypoxia (KV current density decreased from 153.4 ± 9.5 pA / pF to 70.1 ± 10.6 pA / pF at +60 mV), the peak current inhibition rate was (57.6 ± 3.3)%, and the current-voltage curve shifted to the right Move down. (2) The KV current density in chronic intermittent hypoxia group decreased gradually with hypoxia time (there was a significant significance after 10 days of chronic hypoxia), and the current-voltage curve gradually shifted to the right. Acute hypoxia on chronic intermittent hypoxic rat PASMCs KV current inhibition with chronic intermittent hypoxia time and gradually weakened. The above observations suggest that chronic intermittent hypoxia attenuates the inhibition of KV by acute hypoxia, which may be an important mechanism of hypoxia adaptation in the body.