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以往的研究已证明，一氧化氢、前列环素和ATP敏感K+通道均参与低氧性脑血管扩张作用，然而它们之间的相互作用关系尚不清楚，这是本研究的目的．研究用初生小牛基底动脉血管条，观察低氧下（灌流溶液的氢分压为6．0kPa．二氧化碳分任为4．7kPa，pH为7．40±0．02）一氧化氮与前列环素，前列环素与ATP敏感K+通道及ATP敏感K+通道与一氧化氮在脑血管扩张反应申的相互关系．实验结果发现，一氧化氮对前列环素的作用无明显影响．而一氧化氮的作用似乎有赖于前列环素的存在；前列环素对ATP敏感K+通道的活动影响不大，而前列环素对脑血管的作用可能有赖于ATP敏感K+通道；一氧化氮的作用可能不是直接借助于ATP敏感K+通道的作用，ATP敏感K+通道的抑制对一氧化氮也无明显的影响。上述结果提示．在三种扩血管因素中，唯有ATP敏感K+通道的开放所引起的扩血管反应设有受内皮细胞产生的一氧化氮和前列环素两个因子的明显影响，而其化两因子之间有相互的影响作用．
Previous studies have demonstrated that both H 2 O 3, prostacyclin and ATP-sensitive K + channels are involved in hypoxic cerebral vasodilation but the relationship between them is unclear and this is the purpose of this study. Study the use of primary calf basilar artery strips to observe hypoxia (perfusion solution hydrogen partial pressure of 6.0kPa carbon dioxide was 4.7kPa, pH 7.40 ± 0.02) of nitric oxide and the Prostate ring Interrelationships between the Prostacyclin and the ATP Sensitive K + Channels and the ATP Sensitive K + Channels and Nitric Oxide in Cerebrovascular Dilatation. The experimental results showed no significant effect of nitric oxide on prostacyclin. The role of nitric oxide seems to depend on the presence of prostacyclin; prostacyclin has little effect on ATP-sensitive K + channel activity, and the effect of prostacyclin on cerebrovascular may depend on ATP-sensitive K + channels; nitric oxide The effect may not be directly mediated by ATP-sensitive K + channels, and inhibition of ATP-sensitive K + channels has no significant effect on nitric oxide. The above results suggest. Of the three vasoconstrictors, only vasodilator responses caused by the opening of the ATP-sensitive K + channels are markedly affected by two factors, nitric oxide and prostacyclin, produced by endothelial cells, Have mutual influence.