摘要
目的与方法 :采用阻断剂及离体肺内动脉血管环方法 ,研究不同类型钾离子通道对慢性低压低氧的大鼠模型的低氧性肺血管收缩反应 (HPV)的作用 ,旨在探讨钾离子通道在慢性低氧肺血管低反应机制中的作用。结果 :①慢性低氧 15d、3 0d可降低肺血管对急性低氧的收缩反应。②分别阻断正常对照组、慢性低氧组大鼠肺血管钙激活性钾通道 (KCa)、ATP敏感的钾通道 (KATP) ,均使其HPV反应明显增强 ,其中慢性低氧组增强幅度显著高于正常对照组 (P <0 0 1)。③阻断正常对照组、慢性低氧组大鼠肺血管延迟整流性钾通道 (KDR)对其HPV均无明显影响。结论 :KCa、KATP在HPV反应起着重要的调节作用 ,慢性低氧可使此调节作用显著加强 ,这可能是导致肺血管低反应一个重要机制。
AIM and METHODS: To determine the role of different K +-channels in attenuation of vasoreactivity of intrapulminary artery rings induced by chronic hypoxia. RESULTS: ①Acute hypoxia-induced pulmonary vasoconstriction(HPV) could be significantly attenuated by chronic hypobaric hypoxia for 15 days and for 30 days. ②HPV could be significantly potentiated by ATP-sensitive K +-channel (K ATP ) blocker or Ca 2+ -activated K +-channel (K Ca )blocker, and the potentiated scope in chronic hypoxic group was much higher than that observed in control group. ③ Delayed rectifier K +-channel (K DR )blocker showed no effect on HPV in both control group and chronic hypoxic group.CONCLUSIONS: Both K ATP and K Ca play an important modulating role in HPV and it's potentiation may be a critical mechanism for the attenuated vasoreactivity to acute hypoxia; following chronic hypobaric hypoxia.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2001年第10期960-963,共4页
Chinese Journal of Pathophysiology
基金
国家自然科学基金重点资助项目 (No .3 973 0 190 )
