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目的探讨钾离子通道 TASK-1、TASK-3在大鼠睡眠呼吸暂停发生中的可能作用。方法对自由活动的 SD 大鼠进行睡眠呼吸监测。采用 Western 印迹的方法检测不同大鼠脑干TASK-1和 TASK-3的蛋白表达水平,并分析其与睡眠呼吸暂停指数的相关性。建立持续性和间歇性缺氧大鼠模型,分析缺氧对 TASK-1和 TASK-3表达的影响。结果正常 SD 大鼠总自发呼吸暂停(SP)指数、NREM 期自发呼吸暂停指数与脑干中 TASK-1蛋白的表达量成正相关(r 值分别为0.547,0.601,均 P<0.01),而叹息后呼吸暂停(PS)指数与 TASK-1表达量无关。自发呼吸暂停指数和叹息后呼吸暂停指数均与 TASK-3的表达量无相关性(P>0.05)。间歇性缺氧伴高碳酸血症可以使TASK-1、TASK-3 在脑干中的表达增加。结论 TASK-1在大鼠呼吸中枢表达量的增加可能参与了睡眠呼吸暂停的发生。间歇性缺氧伴高碳酸血症可上调 TASK-1、TASK-3的表达。
Objective To investigate the possible role of potassium channel TASK-1 and TASK-3 in the development of sleep apnea in rats. Methods Free-living SD rats were monitored for sleep respiration. The protein expression levels of TASK-1 and TASK-3 in different rat brainstem were detected by Western blotting and their correlations with sleep apnea index were analyzed. To establish a continuous and intermittent hypoxia rat model to analyze the impact of hypoxia on TASK-1 and TASK-3 expression. Results The spontaneous apnea (SP) index of normal SD rats and the spontaneous apnea index of NREM were positively correlated with the expression of TASK-1 protein (r = 0.547,0.601, P <0.01, respectively) Post-apnea (PS) index was independent of TASK-1 expression. Both spontaneous apnea index and post-prandial apnea index had no correlation with the expression of TASK-3 (P> 0.05). Intermittent hypoxia with hypercapnia can make TASK-1, TASK-3 expression in the brain stem increased. Conclusion The increased expression of TASK-1 in the respiratory center of rats may be involved in the occurrence of sleep apnea. Intermittent hypoxia with hypercapnia can up-regulate TASK-1, TASK-3 expression.