缺氧复氧对家兔胸主动脉环张力的影响及其机制

EFFECT OF HYPOXIAREOXYGENATION ON TENSTION OF RABBIT AORTIC RINGS AND ITS MECHANISM

生物测定法观察家兔胸主动脉环经缺氧－复氧后血管张力的变化及这种变化与内皮的关系，并初步探讨了缺氧复氧对血管张力影响的机制。结果表明急剧缺氧可使苯肾上腺素（ＰＥ）预收缩的主动脉环出现短暂的收缩，随即自发舒张，复氧后立即舒张，随后持续收缩；去除内皮或经一氧化氮（ｎｉｔｒｉｃｏｘｉｄｅ，ＮＯ）合成酶抑制剂Ｎ－硝基－精氨酸－甲基酯（Ｌ－ＮＡＭＥ）或鸟苷酸环化酶抑制剂美蓝（ＭＢ）孵育后的血管环，缺氧性收缩反应消除或明显抑制，复氧性舒张也受到明显抑制，而复氧性收缩显著增强；加入ＮＯ合成底物Ｌ－精氨酸（Ｌ－Ａｒｇ）孵育后，有内皮血管环缺氧复氧性张力变化与对照组相比无明显变化。表明缺氧性血管收缩是内皮依赖性的，与ＮＯ释放的迅即减少有关；复氧早期引起的舒张是由于内皮释放ＮＯ引起的，而随后的收缩可能因复氧后大量氧自由基灭活ＮＯ所致。

? Exposure of endotheliuminact precontracted aorta rings to hypoxia resulted in a rapid,transient contraction,followed by relaxation.Reoxygenation initiated relaxation followed by contraction.Removal of endothelium or pretreated with LNAME,MB abolished or markedly decreased the magnitude of contraction induced by hypoxia and relaxation induced by reoxygenation,but potentiated contraction induced by reoxygenation.These results indicated that the characteristic of contraction after hypoxia was endotheliumdependent.The early relaxation of reoxygenation appeared to be due to nitric oxide(NO) release from EC,the followed contraction was related to the degradation of NO by free radicals.