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为了观察急性低压缺氧对肾小球、肾小管和肾血管内皮细胞的损害及其脂质过氧化与血小板活化因子(PAF)两大有害因素在这种损害中的作用,对62只Wistar大鼠进行了急性压缺氧实验,和PAF拮抗剂Taponin的急性低压缺氧干预试验.结果发现,急性低压缺氧后,大鼠血清BUN含量明显升高(P<0.001),肾组织中的ET含量明显下降(P<0.05),血清AKP活性无显著变化(P>0.05).肾组织中SeGSHpx活力明显下降(P<0.001),但MDA含量无明显升高(P>0.005.经PAF拮抗剂Taponin灌胃给药4天,再进行急性低压缺氧实验,发现大鼠血清BUN、Cr及AKP均无明显改变(P>0.05).结果提示,①急性低压缺氧可引起肾小球滤过功能和肾血管内皮细胞的损害.但对肾小管的功能影响不明显.②脂质过氧化损害不是急性低压缺氧时肾功能改变的主要原因.③PAF拮抗剂Taponin对急性重度低压缺氧引起的肾损害有明显的保护作用,说明急性低压缺氧时体内有过多的PAF释放并在肾损害中有重要作用.
To observe the effect of acute hypobaric hypoxia on glomerular, tubular and renal vascular endothelial cell damage and the two harmful factors of lipid peroxidation and platelet activating factor (PAF) in this lesion, 62 Wistar rats The rats were subjected to an acute hypobaric hypoxia test and an acute hypobaric hypoxia intervention test with the PAF antagonist Taponin.The results showed that serum BUN levels were significantly increased (P <0.001) in acute hypobaric hypoxia and ET (P <0.001), but the content of MDA was not significantly increased (P> 0.05) .Conclusion: PAF antagonist can inhibit the activity of SeGSHpx in renal tissue significantly (P <0.05) Taponin intragastric administration for 4 days, and then acute hypobaric hypoxia experiments found no significant changes in serum BUN, Cr and AKP (P> 0.05) .The results suggest that ① acute hypobaric hypoxia can cause glomerular filtration Function and renal vascular endothelial cell damage, but no significant effect on the tubular function.②Peripheral lipid peroxidation damage is not the main reason of acute hypoxia and renal dysfunction.③Paponin antagonist of acute severe hypobaric hypoxia caused Kidney damage has a significant protective effect, indicating acute hypoxia When the body has too much PAF release and have an important role in renal injury.