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目的:研究急性缺氧对大鼠肺动脉平滑肌细胞电压门控钾通道(Kv)电流的影响。方法:雄性SD大鼠20只随机分为常氧对照组和急性缺氧组(各10只)。急性缺氧组大鼠在低氧仓中缺氧停留8 h后进行实验。应用全细胞膜片钳技术记录肺动脉平滑肌细胞电压门控钾通道电流(IK)。结果:急性缺氧显著降低大鼠肺动脉平滑肌细胞的IK密度。在大鼠肺动脉平滑肌细胞静息膜电位-60 mV至-10mV时,急性缺氧降低大鼠肺动脉平滑肌细胞的IK密度不明显(P>0.05)。在0mV时,大鼠肺动脉平滑肌细胞的峰值IK密度显著下降[从(38.1±5.2)pA/pF→(9.82±2.1)pA/pF,P<0.05)],此后随着细胞静息膜电位的增加,平滑肌细胞的IK密度下降幅度逐渐增加(P<0.05);从+30 mV至+60 mV时,平滑肌细胞的IK密度下降幅度更大(P<0.01)。在+60 mV时,IK密度峰值从(135.4±16.5)pA/pF降到(73.1±10.6)pA/pF,降幅达(46.8±3.3)%。结论:急性缺氧可降低肺动脉平滑肌细胞Kv电流,导致肺血管缺氧性收缩。
AIM: To investigate the effect of acute hypoxia on voltage-gated potassium channel (Kv) currents in rat pulmonary artery smooth muscle cells. Methods: Twenty male SD rats were randomly divided into normoxia control group and acute hypoxia group (n = 10 each). Rats in acute hypoxia group were subjected to hypoxia for 8 hours in hypoxia chamber. Whole cell patch clamp technique was used to record voltage-gated potassium current (IK) of pulmonary artery smooth muscle cells. Results: Acute hypoxia significantly reduced IK density in rat pulmonary artery smooth muscle cells. Acute hypoxia decreased the IK density of pulmonary artery smooth muscle cells in rat pulmonary arterial smooth muscle cells at resting membrane potential of -60 mV to -10 mV (P> 0.05). At 0 mV, the peak IK density of rat pulmonary artery smooth muscle cells significantly decreased from (38.1 ± 5.2) pA / pF to (9.82 ± 2.1) pA / pF, P <0.05) (P <0.05). From +30 mV to +60 mV, the IK density of smooth muscle cells decreased more significantly (P <0.01). At +60 mV, peak IK densities decreased from (135.4 ± 16.5) pA / pF to (73.1 ± 10.6) pA / pF, a decrease of 46.8 ± 3.3%. Conclusion: Acute hypoxia can reduce the Kv current of pulmonary artery smooth muscle cells, resulting in pulmonary vascular hypoxic contraction.