Tubular function in glycerol-induced acute renal failure in rats: effect of saline loading and prior acute renal failure.
Tubular function in glycerol-induced acute renal failure in rats: effect of saline loading and prior acute renal failure.
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甘油诱导的大鼠急性肾衰竭的肾小管功能：盐水负荷和先前急性肾衰竭的影响。
DOI：
10.1042/cs0620667
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
Kurtzman,NA
中科院分区：
文献类型：
--
作者：
Westenfelder,C;Crawford,PA;Hamburger,RK;Baranowski,RL;Kurtzman,NA
1.慢性生理盐水负荷和急性肾衰竭的预先诱导是已报告的防止急性肾衰竭发展的策略。潜在的机制尚不清楚。本研究的目的是在甘油诱导的急性肾衰竭模型中检查这些保护性操作对肾小球滤过率（GFR）和近端和远端肾小管功能的影响.诱导急性肾衰竭（50%甘油，10 ml/kg体重）。肌内注射）在三组大鼠中进行：第1组，饮水;第2组，生理盐水负荷（1%NaCl作为饮用液，持续5周）;第3组，在第一次甘油给药后7-15天，当血液尿素氮水平恢复正常时再激发。第3组中的对照动物仅接受第一次甘油注射，然后，与第1组和第2组中的对照一样，向其给予0.9% NaCl溶液（10 ml/kg体重）。肌内注射）。然后在甘油或盐水注射后24小时对所有动物进行研究。甘油导致所有三组的GFR显著下降（第1组78%;第2组64%;第3组59%）;血尿素氮水平显著升高。盐水负荷的急性肾功能衰竭动物（第2组）表现出糖尿，血糖水平正常，最大肾小管葡萄糖重吸收显著降低。重吸收HCO− 3的能力在HCO− 3负荷之前和期间都受到抑制。在HCO− 3负荷期间（尿液pH 7.8），通过尿-血Pco 2梯度（U-BPco 2）评估的远端酸化正常。高氯血症代谢性酸中毒的存在表明这些动物发生了近端肾小管酸中毒。甘油再注射的急性肾功能衰竭大鼠（第3组）正常重吸收葡萄糖和HCO− 3，并显示正常的远端小管酸化。我们从这些数据中得出结论，急性肾功能衰竭的前一次发作保护近端小管免受第二次甘油挑战，而慢性盐水负荷没有这种保护作用。这种肾小管细胞抵抗（针对第二次甘油挑战）的潜在机制和近端肾小管功能在急性肾衰竭发病机制中的作用仍不清楚。
1. Chronic saline loading and prior induction of acute renal failure are manoeuvres which have been reported to protect against the development of acute renal failure. The underlying mechanisms are unclear. The purpose of the present study was to examine the effect of these protective manoeuvres on glomerular filtration rate (GFR) and proximal and distal tubular function in the glycerol-induced model of acute renal failure.2. Acute renal failure was induced (50% glycerol, 10 ml/kg body wt. intramuscularly) in three groups of rats: group 1, water drinking; group 2, saline loaded (1% NaCl as drinking fluid for 5 weeks); group 3, rechallenged 7–15 days after a first dose of glycerol, when blood urea nitrogen levels had returned to normal. Control animals in group 3 received only the first glycerol injection, then, like the controls in groups 1 and 2, they were given 0.9% NaCl solution (10 ml/kg body wt. intramuscularly). All animals were then studied 24 h after glycerol or saline injection.3. Glycerol caused a significant fall in GFR in all three groups (78% group 1; 64% group 2; 59% group 3); blood urea nitrogen levels rose significantly. Saline-loaded animals with acute renal failure (group 2) exhibited glycosuria with normal blood-sugar levels and a striking depression in maximal tubular glucose reabsorption. The capacity to reabsorb HCO−3was depressed both before and during HCO−3loading. Distal acidification as assessed by the urine to blood gradient ofPco2(U—BPco2) was normal during HCO−3loading (urine pH 7.8). The presence of hyperchloraemic metabolic acidosis demonstrated that these animals developed proximal renal tubular acidosis. Glycerol-reinjected rats with acute renal failure (group 3) reabsorbed glucose and HCO−3normally and exhibited normal distal tubule acidification.4. We conclude from these data that a prior episode of acute renal failure protects proximal tubules against a second glycerol challenge, whereas chronic saline loading is without this protective effect. Both the underlying mechanism for this tubular cell resistance (against a second glycerol challenge) and the role of proximal tubular function in the pathogenesis of acute renal failure remain unclear.
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DOI：
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DOI：
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