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胎鼠急性缺血/再灌注损伤肾NO及NOS的改变 被引量:4

EFFECT OF ACUTE ISCHEMIA-REPERFUSION ON NITRIC OXIDE AND NITRIC OXIDE SYNTHASE IN FETAL RAT KIDNEY
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摘要 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 effct of acute ischemia-reperfusion on nitric oxide and nitric oxide synthasc in fetal rat kidney, Using arterial clamp occluded one side of vessels supplying uterus and ovary in pregnant 21 days Wistar rats. The level of NO and acticity of NOS were detected by biochenistry and immunohistochenistry methods respectively. Results showed that the contents of NO decreased gradually with extension of ischemia which was significance comparing with sham group(P < 0.01) . During reperfusion stage the contents of NO were low at first and then increased, espeecially in 30 minutes ischemia groups. eNOS and iNOS all expressed in proximal tubules in sham operation group. With the extension of ischemia and reperfusion the intensity of eNOS increased progressively especially in reperfused group after 30 minutes' ischemia. The trend of iNOS was oppositive to that of eNOS espeecially in 30 minutes ischemia groups. On conclusion, the changes of NO indicate that NO participate in renal injury duiong ischenia-reperfusion properly. The alternation of NO contents may be composite influence of eNOS and iNOS.
作者 韩梅 魏克伦
出处 《新生儿科杂志》 2002年第3期116-119,共4页 The Journal of Neonatology
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