Shanley P F, Brezis M, Spokes K, Silva P, Epstein F H, Rosen S
Am J Kidney Dis. 1986 Jan;7(1):76-83. doi: 10.1016/s0272-6386(86)80059-2.
Rat kidneys were perfused for 90 minutes with cyanide, rotenone, antimycin, 2-deoxyglucose, or combinations of rotenone or antimycin with 2-deoxyglucose in oxygenated Krebs-albumin medium. Following perfusion, proximal tubule injury was evaluated by light microscopy. The types of lesions seen were similar to those previously reported after hypoxic perfusion and included brush border clubbing/mitochondrial swelling in S1 and S2 and cytoplasmic edema or cell fragmentation in S3. This finding supports the contention that these lesions represent characteristic responses of these segment types and that the S3 response differs from that in S1 and S2. S1 appeared most vulnerable to low dose cyanide or inhibition of mitochondrial electron transport (rotenone, antimycin). Inhibition of glycolysis (2-deoxyglucose) only produced injury in S2 tubules. With high dose cyanide or a combination of 2-deoxyglucose with either rotenone or antimycin, there was diffuse proximal tubule damage. Thus S3 appeared more resistant than the convoluted tubular segments to both inhibition of glycolysis and to inhibition of mitochondrial electron transport. This finding stands in contrast to the selective vulnerability of the S3 segment in ischemic renal injury.
在含氧的 Krebs - 白蛋白培养基中,用氰化物、鱼藤酮、抗霉素 A、2 - 脱氧葡萄糖,或鱼藤酮或抗霉素 A 与 2 - 脱氧葡萄糖的组合对大鼠肾脏进行 90 分钟的灌注。灌注后,通过光学显微镜评估近端小管损伤。观察到的病变类型与先前缺氧灌注后报道的相似,包括 S1 和 S2 段的刷状缘杵状变/线粒体肿胀以及 S3 段的细胞质水肿或细胞破碎。这一发现支持了以下观点:这些病变代表了这些节段类型的特征性反应,并且 S3 段的反应不同于 S1 和 S2 段。S1 段似乎对低剂量氰化物或线粒体电子传递抑制(鱼藤酮、抗霉素 A)最为敏感。糖酵解抑制(2 - 脱氧葡萄糖)仅在 S2 小管中产生损伤。使用高剂量氰化物或 2 - 脱氧葡萄糖与鱼藤酮或抗霉素 A 的组合时,近端小管出现弥漫性损伤。因此,S3 段似乎比曲管段对糖酵解抑制和线粒体电子传递抑制都更具抗性。这一发现与缺血性肾损伤中 S3 段的选择性易损性形成对比。