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用超氧化物歧化酶和蔗糖预防缺血性急性肾衰竭。

Prevention of ischaemic acute renal failure with superoxide dismutase and sucrose.

作者信息

Bayati A, Hellberg O, Odlind B, Wolgast M

出版信息

Acta Physiol Scand. 1987 Jul;130(3):367-72. doi: 10.1111/j.1748-1716.1987.tb08150.x.

Abstract

The preventive effects of intravenously administered superoxide dismutase (SOD) and of SOD combined with sucrose on acute renal failure were investigated in rat kidneys exposed to 45 min of warm ischaemia. Superoxide dismutase (20 mg) given just before primary ischaemia and in the early recirculation phase was found to ameliorate the red cell aggregation in the renal medulla, in particular, in the inner stripe of the outer zone the volume of trapped red cells decreased from 11.2 +/- 1.6% in untreated animals to 0.02 +/- 0.001%, thus allowing improved restoration of medullary blood flow. This was also accompanied by an expected restoration of the urine osmolality reaching almost 400 mOsm kg-1 after administration of SOD + sucrose. Superoxide dismutase also restored the capillary macromolecular permeability as evidenced by normalization of plasma to lymph transport of proteins. Micropuncture studies showed that in ischaemically damaged but untreated kidneys the tubules were obstructed and that the proximal tubular pressure rose to such a level that the net driving force for filtration approached zero. This explains the marked decrease in glomerular filtration rate (GFR) from a normal value of about 1 ml min-1 to 0.01 +/- 0.02 ml min-1. After treatment with SOD the tubules were still largely obstructed, resulting in a depression of the net driving force and a decrease in single nephron glomerular filtration rate (SNGFR) to about 11 nl min-1, that is, to only 25% of the normal SNGFR. The total filtration was 0.09 +/- 0.04 ml min-1.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在经历45分钟热缺血的大鼠肾脏中,研究了静脉注射超氧化物歧化酶(SOD)以及SOD与蔗糖联合使用对急性肾衰竭的预防作用。发现在初次缺血前和再灌注早期给予超氧化物歧化酶(20毫克)可改善肾髓质中的红细胞聚集,特别是在外带的内条纹中,被困红细胞的体积从未经治疗动物的11.2±1.6%降至0.02±0.001%,从而使髓质血流的恢复得到改善。这还伴随着尿渗透压的预期恢复,在给予SOD +蔗糖后尿渗透压几乎达到400 mOsm/kg。超氧化物歧化酶还恢复了毛细血管大分子通透性,这可通过血浆至淋巴的蛋白质转运正常化得到证明。微穿刺研究表明,在缺血受损但未经治疗的肾脏中,肾小管受阻,近端肾小管压力升高至使滤过的净驱动力接近零的水平。这解释了肾小球滤过率(GFR)从正常值约1毫升/分钟显著降至0.01±0.02毫升/分钟。用SOD治疗后,肾小管仍大部分受阻,导致净驱动力降低,单肾单位肾小球滤过率(SNGFR)降至约11纳升/分钟,即仅为正常SNGFR的25%。总滤过率为0.09±0.04毫升/分钟。(摘要截短于250字)

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