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目的 :探讨K+ 通道在慢性低氧致低氧性肺血管收缩反应降低中的作用。方法 :采用离体肺灌流实验 ,研究 4-AP(4-aminopyridine ,电压依赖性K+ 通道 -Kv阻滞剂 )、TEA(tetraethylamonium ,Ca2 + 激活性K+ 通道 -KCa阻滞剂 )、GLIB(glibenclamide,ATP敏感性K+ 通道 -KATP阻滞剂 )对正常与慢性低氧大鼠肺血管低氧反应的影响。结果 :4-AP、TEA均可使正常大鼠肺动脉基础压上升 ,且使其肺血管低氧反应明显增强 ;对于慢性低氧大鼠 ,其肺血管对低氧反应明显低下 ,4-AP、TEA升肺动脉基础压的作用明显低于对照鼠肺 ,GLIB也呈现升高肺动脉基础压力作用 ,4-AP、TEA、GLIB均可使肺血管低氧反应大大增强 ,增强的比例明显大于正常对照组。结论 :在离体灌流鼠肺HPV中 ,Kv、KCa的开放起调节作用 ,大鼠经慢性低氧后 ,肺血管反应性明显降低 ,可能与Kv、KCa、KATP在HPV中的调节作用相对增强有关
Objective: To investigate the role of K + channel in the reduction of hypoxic pulmonary vasoconstriction induced by chronic hypoxia. Methods: The effects of 4-aminopyridine (K-channel blocker), TEA (tetraethylamonium), Kib channel blocker (KA) and GLIB (glibenclamide) , ATP - sensitive K + channel - KATP blocker) on pulmonary vascular hypoxic response in normal and chronic hypoxia rats. Results: 4-AP, TEA can make the pulmonary artery in normal rats increased basal pressure, and pulmonary vascular hypoxia response was significantly enhanced; chronic hypoxic rat pulmonary vascular hypoxia response was significantly lower, 4-AP, TEA and GLIB significantly increased the pulmonary vascular hypoxia response, and the proportion of enhancement was significantly greater than that of the normal control group . CONCLUSION: Kv and KCa play a regulatory role in the in vitro perfusion of murine lung HPV. The pulmonary vascular reactivity is significantly decreased after chronic hypoxia in rats, which may be related to the regulation of Kv, KCa and KATP in HPV related