论文部分内容阅读
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。
The bioassay was used to observe the changes of vascular tone after hypoxia-reoxygenation in rabbit thoracic aorta ring and the relationship between the changes and the endothelium. The mechanism of hypoxia-reoxygenation on vascular tone was also discussed. The results showed that acute hypoxia induced short-term contraction of pre-contracted aortic rings of phenylephrine (PE), then spontaneously diastolic, diastolic immediately after reoxygenation and then continued to contract; removal of endothelial or nitricoxide (NO) Vascular rings after incubation with the synthetase inhibitor N-nitro-arginine-methyl ester (L-NAME) or guanylate cyclase inhibitor methylene blue (MB) resulted in the elimination or significant inhibition of hypoxic contractile responses , Reoxygenation relaxation was also significantly inhibited, and reoxygenation contraction was significantly enhanced; adding NO synthesis substrate L-arginine (L-Arg) incubated with endothelial vascular hypoxia reoxygenation tension changes and the control group No significant change compared to. Suggesting that hypoxic vasoconstriction is endothelium-dependent, with the rapid reduction of NO release; reoxygenation caused by diastolic early release of NO due to endothelial, and subsequent contraction may be a large number of oxygen free radicals after reoxygenation of NO Due.