中文摘要：

目的 探讨慢性间歇性低压低氧（chronic intermittent hypobaric hypoxia,CIHH）对大鼠心室肌细胞瞬时外向钾通道电流（transient outward potassium channel current,Ito）和稳态外向钾通道电流（steady-state outward potassium channel current,Iss）的影响.方法 通过低压氧舱制备CIHH大鼠模型,全细胞膜片钳方法 记录大鼠心室肌细胞Ito和Iss.结果 基础条件下,28d CIHH处理大鼠心室肌细胞Ito电流密度较对照组大鼠心室肌细胞明显增强（P＜0.05）,而Iss电流密度与对照组大鼠心室肌细胞相比较差异无统计学意义（P＞0.05）.模拟缺血可明显降低大鼠心室肌细胞Ito和Iss（P＜0.05）,但CIHH处理大鼠心室肌细胞Ito的降低明显小于对照组大鼠心室肌细胞（P＜0.05）,而Iss的降低与对照组心室肌细胞差异无统计学意义（P＞0.05）.结论 CIHH可增强大鼠心肌细胞Ito通道电流,并有效对抗模拟缺血对Ito通道的抑制,此作用可能是CIHH抗心律失常作用的离子机制之一.

英文摘要：

Objective To observe the effect of chronic intermittent hypobaric hypoxia （CIHH） on transient outward potassium channel current （Ito） and steady-state outward potassium channel current （lss） in ventricular myocytes of rats. Methods The rats were treated with CIHH for 28 days in a hypobaric chamber and the whole-cell patch clamp technique was used to record Ito and Iss in ventricular myocytes of rats. Results Compared with the control rats, the current density of Ito in the CIHH rats under basic conditions increased significantly （P 〈 0.05 ）. There was no significant difference in the current density of Iss between the two groups （ P 〉 0.05 ）. The simulated ischemia decreased Ito and Iss obviously in ventricular myocytes of rats （ P 〈 0.05 ）. The decrease of Ito in CIHH rats was significantly less than that in control rats （P 〈 0.05 ）, but there was no difference in Iss between the two groups （P 〉 0. 05）. Conclusion CIHH increased Ito current and effectively antagonized the inhibition of simulated ischemia on Ito channel in ventricular myocytes of rats, which might be one of the ionic mechanisms of anti-arrhythmia of CIHH.