导致肺、脑血管缺氧反应差异的因素  

Factors accounting for different response of pulmonary and cerebral vessels to hypoxia

作　　者：王迪浔[1] 金咸瑢[1] 刘声远[1] 万有[1] 李会革[1] 彭远开[1] 刘杰[1] 胡宏镇[1] 张业平[1] 

机构地区：[1]同济医科大学卫生部呼吸系疾病重点实验室,武汉430030

出　　处：《中国病理生理杂志》1997年第4期341-346,共6页Chinese Journal of Pathophysiology

基　　金：国家八五攻关项目

摘　　要：大鼠,家兔和狗整体实验研究交感神经、感觉神经肽、花生四烯酸环氧合酶及脂氧合酶代谢产物,内皮源性舒张因子,活性氧和钾通道在缺氧性肺血管收缩(HPV)和脑血管舒张反应(HCVD)中的作用。结果发现缺氧时,交感神经收缩肺,脑血管;感觉神经肽、内皮源性舒张因子和4-AP敏感性钾通道的开放均使肺、脑血管舒张;环氧合酶代谢产物舒张肺血管和收缩脑血管,而脂氧合酶代谢产物则收缩肺血管和舒张脑血管。缺氧使肺组织活性氧减少从而促使肺血管收缩,而脑组织活性氧含量无明显变化;ATP敏感性钾通道关闭致肺血管收缩,而在脑血管反应中无作用。结果表明,在这些因子中主要是脂氧合酶代谢产物、活性氧和ATP敏感性钾通道的变化介导HPV,并介导或不影响HCVD,为导致肺、脑血管对缺氧反应差异的因素。Roles of sympathicus, sensory neuropeptides (SNP), metabolites of cyclooxygenase, metabolites of lipoxygenase, endothelium derived relaxing factor (EDRF), reactive oxygen (ROS) and potassium channels (PC) in the hypoxic pulmonary vasoconstriction (HPV) and hypoxic cerebral vasodilation (HCVD) were studied in intact rats, rabbits and dogs. Results were as follows: during hypoxia, the excitation of sympathicus results in a constriction of both pulmonary and cerebral vessels; SNP, EDRF and the opening of 4-AP sensitive PC caused the dilation of both of them; metabolites of lipoxygenase mediated HPV and HCVD, whereas metabolites of cyclooxygenase were their modulators; hypoxia induced blockade of the ATP sensitive PC mediated HPV, but had no effect on HCVD; reduction of O_2^+ in the lung might potentiate HPV, but had no effect on HCVD. It is suggested that the alteration of lipoxygenase metabolites, ROS and ATP sensitive PC are factors accounting for the difference in response of pulmonary and cerebral vassels to hypoxia.

关 键 词：缺氧症 肺循环 脑血管循环 

分 类 号：R364.4[医药卫生—病理学]