【摘要】 目的：观察缺氧复氧对肾性高压（ｒｅｎａｌ ｈｙｐｅｒｔｅｎｓｉｏｎ ， ＲＨ） 组及假手术（ｃｏｎｔｒｏｌ ， Ｃ） 组大鼠血管舒缩反应的影响，并对其机制进行了初步探讨。方法：采用Ｇｏｌｄｂｌａｔｔ 方法复制ＲＨ 大鼠模型，并应用离体血管灌流方法观察血管舒缩反应的变化。结果：缺氧可引起对照组大鼠有内皮主动脉环产生一快速、短暂的额外收缩，随后舒张。复氧可使其先舒张、后收缩。ＲＨ 组大鼠胸主动脉缺氧性收缩及复氧性舒张减弱，而随后的收缩增强。Ｎ－ 硝基－ Ｌ－ 精氨酸甲基酯（Ｎ－ ｎｉｔｒｏ － Ｌ－ ａｒｇｉｎｉｎｅ － ｍｅｔｈｙｌｅｓｔｅｒ ， Ｌ－ ＮＡＭＥ） 可减弱缺氧收缩及复氧舒张、增强复氧收缩。超氧化物歧化酶（ｓｕｐｅｒｏｘｉｄｅ ｄｉｓｍｕｔａｓｅ ，ＳＯＤ） 可提高复氧舒张，减弱复氧收缩，ＲＨ 组减弱明显。结论：ＲＨ 组大鼠胸主动脉缺氧复氧舒缩反应变化与内皮分泌内皮源性舒张因子（ｅｎｄｏｔｈｅｌｉｕｍ － ｄｅｒｉｖｅｄ ｒｅｌａｘｉｎｇ ｆａｃｔｏｒ ， ＥＤＲＦ） 机制受损及自由基生成增多有关更多还原

【Abstract】 AIM and METHOD:The effect of hypoxia-reoxygenation on vasoconstriction and vasodilation of thoracic artery in renal hypertensive (RH) rats were observed by bioassay and its mechanism was investigated and compared with those age-matched controls(C).RESULTS:Anoxia caused a prompt endothelium-dependent contraction followed by relaxation. However reoxygenation resulted in a transient relaxation followed by contraction. The anoxia-mediated contraction in RH group. The pretreatment with L-NAME decreased the anoxic contation and reoxygenation and reoxygenation relaxation was reduced, accompanied by an increased reoxygenation contraction dilation, exaggerated the reoxygenation contraction. In contrast, the addition of superoxide dismutase (SOD) just before reoxygenation could significantly improve reoxygenation dilation and decreased reoxygenation contraction in RH groups. CONCLUSION:The damaged EDRF releasing and the production of superoxide radicals might play roles in the hypoxia and/or reoxygenation-mediated relaxation and contraction.更多还原