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研究宫内急性缺血缺氧及再灌注时胎鼠肾NO水平及NOS活性变化,以无创动脉夹钳夹孕鼠供应子宫和卵巢的动静脉血管,制成宫内急性缺血缺氧及再灌注模型。以硝酸还原酶法和免疫组化法测定胎鼠肾NO水平和NOS活性变化。结果显示随缺血缺氧时间延长NO水平明显降低,与假手术组相比,差异显著P<0.01。随再灌注时间延长NO水平呈双向改变,尤为缺血缺氧30分钟组。正常时eNOS和iNOS即位于近曲小管。随缺血缺氧及再灌注时间的延长,eNOS光强度逐渐升高,iN-OS光强度逐渐显著减弱,尤为缺血缺氧30分钟再灌注组。表明NO的动态变化可能参与缺血缺氧再灌注损伤过程。缺血缺氧及再灌注后肾NO水平的双相改变可能是eNOS和iNOS活性变化的综合结果。
To study the intrauterine acute ischemia, hypoxia and reperfusion of fetal rat kidney NO levels and changes in NOS activity, with non-invasive artery clamp to supply uterine and ovarian mothers venous blood vessels, made intrauterine acute ischemia and hypoxia and then Perfusion model. Nitric acid reductase and immunohistochemistry were used to determine the changes of NO and NOS activity in fetal rat kidney. The results showed that with the prolonged ischemia and hypoxia NO levels were significantly lower than the sham operation group, the difference was significant P <0.01. With the reperfusion time prolonged NO levels showed bidirectional changes, especially ischemia and hypoxia 30 minutes group. Normal eNOS and iNOS that is located in the proximal tubule. With the prolongation of ischemia and hypoxia and reperfusion time, the light intensity of eNOS gradually increased, and the light intensity of iN-OS gradually weakened significantly, especially for reperfusion 30 minutes after ischemia and hypoxia. Suggesting that the dynamic changes of NO may be involved in the process of ischemia-reperfusion injury. Biphasic changes of renal NO level after hypoxia-ischemia and reperfusion may be the result of changes of eNOS and iNOS activity.