Transport-dependent cell injury in the S3 segment of the proximal tubule.
Transport-dependent cell injury in the S3 segment of the proximal tubule.
复制标题
近曲小管 S3 段的运输依赖性细胞损伤。
DOI：
10.1038/ki.1986.103
复制
发表时间：
1986
影响因子：
19.6
通讯作者：
Rosen,S
中科院分区：
文献类型：
--
作者：
Shanley,PF;Brezis,M;Spokes,K;Silva,P;Epstein,FH;Rosen,S
近端小管S3段的转运依赖性细胞损伤。在离体缺氧灌流的大鼠肾脏（Krebs-白蛋白培养基中不含O2）中，近端小管S3段发生两种不同类型的损伤，细胞质水肿和细胞碎片。S3小管断裂的比例与GFR和尿量密切相关，当GFR随灌注压升高而升高时，S3小管断裂的比例接近100%。相反，当灌流高钾介质以防止肾小球滤过或在灌流液中加入哇巴因（10- 2 M）抑制肾小管转运时，不存在碎片化损伤，且水肿广泛。多烯抗生素增加膜通透性，从而增加主动电解质转运的工作。在含氧培养基中灌注3 × 10 ~（-5）M的阿替霉素或200 U/ml的制霉菌素也可使S_3产生裂解。在非滤过肾中防止了病变。哇巴因完全消除了制霉菌素引起的细胞碎片，并显着减少了两性霉素引起的细胞碎片。这些结果表明，运输活性增强了细胞碎片的损伤，当运输被抑制时，细胞碎片的损伤减弱。这种水肿与缺血性病变有本质的不同，更类似于缺血性病变，缺血性病变中肾小管血流缺失，主动转运减少，形态学变化似乎与细胞体积调节丧失有关。因此，近端肾小管S3节段表现出的缺氧损伤类型可能是由肾小管细胞的主动离子转运调节的。
Transport–dependent cell injury in the S3segment of the proximal tubule. Two distinct types of injury,cytoplasmic edemaandcell fragmentationoccur in the S3segment of the proximal tubule in isolated hypoxic perfused rat kidneys (Krebs–albumin medium gassed without O2). The proportion of S3tubules withfragmentationstrongly correlated with the GFR and urine output during the perfusion, and approached 100% when the GFR was increased by high perfusion pressure. Conversely, thefragmentationlesion was absent and theedemalesion extensive when tubular transport was inhibited by perfusion with hyperoncotic medium to prevent glomerular filtration or by addition of ouabain (10-2M) to the perfusate. Polyene antibiotics increase membrane permeability and thus the work of active electrolyte transport. Perfusion with amphotericin (3 × 10-5M) or nystatin (200 U/mliter) in oxygenated medium also producedfragmentationin S3. The lesion was prevented in the non-filtering kidney. Ouabain completely eliminated thecell fragmentationdue to nystatin and significantly reduced that due to amphotericin. These results suggest that the injury ofcell fragmentationis enhanced by transport activity and diminished when transport is inhibited. Theedemalesion appears fundamentally different and more akin to lesions described in ischemia where tubular flow is absent, active transport is diminished, and the morphologic changes appear related to loss of cell volume regulation. The type of hypoxic damage exhibited by proximal tubular S3segments may therefore be conditioned by active ion transport of tubular cells.