Bayati A, Källskog O, Wolgast M
Department of Physiology and Medical Biophysics, University of Uppsala, Sweden.
Acta Physiol Scand. 1990 Jan;138(1):25-33. doi: 10.1111/j.1748-1716.1990.tb08809.x.
The long-term outcome in rat kidneys subjected to 45 min of warm ischaemia with no treatment and after administration of 20 mg superoxide dismutase (SOD) and of SOD combined with 2 ml of a 12% sucrose solution was studied by the micropuncture technique. It was found that, although in the acute phase SOD prevented trapping of erythrocytes in the medullary vasculature and that SOD + sucrose also prevented the formation of tubular obstruction, the long-term results as studied 1 week and 1 month after the primary ischaemic insult were virtually identical. This was due to the formation of new obstructions, during the first week, mainly in the thick ascending limb of Henle's loop. After 1 month the proximal tubular free-flow pressure and the single-nephron filtration rate had returned to normal. However, since the total glomerular filtration was only one-third of that under normal conditions, it would seem that two-thirds of the nephrons had undergone complete degeneration. This degeneration was probably the result of persistent tubular obstruction. The tubular degeneration was also accompanied by a reduction in urine osmolality and potassium secretion.
采用微穿刺技术研究了大鼠肾脏在未经处理、给予20毫克超氧化物歧化酶（SOD）以及SOD与2毫升12%蔗糖溶液联合处理后，经历45分钟热缺血的长期结果。结果发现，虽然在急性期SOD可防止红细胞在髓质血管系统中滞留，且SOD+蔗糖也可防止肾小管梗阻的形成，但在初次缺血损伤后1周和1个月时研究的长期结果基本相同。这是由于在第一周内主要在髓袢升支粗段形成了新的梗阻。1个月后近端肾小管自由流压力和单肾单位滤过率恢复正常。然而，由于总肾小球滤过率仅为正常条件下的三分之一，似乎三分之二的肾单位已完全退化。这种退化可能是持续性肾小管梗阻的结果。肾小管退化还伴有尿渗透压和钾分泌的降低。
