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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。
General Experimental Study in Rats, Rabbits and Dogs Sympathetic nerves, sensory neuropeptides, arachidonic acid cyclooxygenase and lipoxygenase metabolites, endothelium-derived relaxing factor, reactive oxygen species, and potassium channels in hypoxic pulmonary vessels Contraction (HPV) and cerebral vasodilation (HCVD). The results showed that hypoxia, sympathetic contraction of the lung and cerebrovascular; sensory neuropeptide, endothelium-derived relaxing factor and 4-AP-sensitive potassium channels are open to the lungs, cerebrovascular relaxation; cyclooxygenase metabolites to relax the pulmonary vessels And contracting cerebrovascular, while lipoxygenase metabolites constrict pulmonary and diastolic blood vessels. Hypoxia reduced the reactive oxygen species in the lung tissue and induced vasoconstriction in the pulmonary vasoconstrictor, while there was no significant change in reactive oxygen species in the brain tissue. The ATP-sensitive potassium channels closed to pulmonary vasoconstriction, but no effect in the cerebrovascular response. The results indicate that changes in these factors, mainly lipoxygenase metabolites, reactive oxygen species and ATP-sensitive potassium channels, mediate HPV and mediate or deactivate HCVD, which is responsible for the differential response of lung and cerebrovascular responses to hypoxia factor.