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目的了解缺血时肾小管上皮细胞 (TEC)微丝的改变 ,并探讨此改变的机制。方法用双肾蒂钳夹法建立缺血性急性肾衰模型 ,采用电镜和免疫组化法观察缺血 5、15和 45min时TEC微丝肌动蛋白的改变 ,并用高效液相色谱法测试细胞内三磷酸腺苷 (ATP)水平。结果缺血 5min即有细胞微丝肌动蛋白的损害 ,微绒毛融合、断裂 ,随着缺血时间的延长 ,微丝损伤加重 ,极性丧失 ,由细胞尖端分布变为胞浆内弥漫分布 ,微绒毛消失 ,与此同时细胞内ATP水平也迅速降低 ,微丝紊乱程度与ATP的下降呈一致。结论肾TEC微丝结构和极性的改变可能与细胞内ATP水平相关。
Objective To investigate the change of microfilament of renal tubular epithelial cells (TEC) during ischemia and to explore the mechanism of this change. Methods The model of ischemic acute renal failure was established by double renal pedicle clamp method. The changes of TEC actin filaments were observed by electron microscopy and immunohistochemistry at 5, 15 and 45 min, and the cells were tested by high performance liquid chromatography Adenosine triphosphate (ATP) levels. Results There was damage of actin microfilament and microvilli fusion and rupture at 5min after ischemia. With the extension of ischemic time, the damage of microfilament increased and the polarity was lost. From the tip of the cell to the diffuse distribution in the cytoplasm, Microvilli disappeared, while intracellular ATP levels also decreased rapidly, the degree of disruption and ATP consistent with the decline in ATP. Conclusion The changes of structure and polarity of renal TEC microfilaments may be related to intracellular ATP level.