Renal function studies in an experimental model of papillary necrosis in the rat.
Renal function studies in an experimental model of papillary necrosis in the rat.
复制标题
大鼠乳头坏死实验模型中的肾功能研究。
DOI：
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发表时间：
1981
期刊：
影响因子：
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通讯作者：
S. Ringoir
中科院分区：
文献类型：
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作者：
R. Vanholder;N. Lameire;W. Eeckhaut;S. Ringoir
在大鼠中静脉注射溴乙胺-氢溴酸盐（溴乙胺）后24小时，观察到均匀的乳头坏死。本研究探讨了肾功能和乳头状血流动力学的急性容量扩张（体重的12%），在这个模型中。肾功能研究在缺水和体积扩大假或BEA注射大鼠中进行。在水缺乏的正常动物中，GFR为1.97 +/- 0.14 ml/min，尿渗透压（UOsm）为1011 +/- 94.5 mOsm/kg，钠排泄分数（FENa）为0.18 +/- 0.026%。相比之下，BEA处理的缺水动物显示出较低的GFR（1.16 +/- 0.14 ml/min）、UOsm（469 +/- 30.31 mOsm/kg）和较高的FENa（0.37 +/- 0.06%）。两组在扩容时UOsm和FENa相似。采用白蛋白累积法测定各组乳头状血浆流量（PPF）。在水缺乏的正常动物中，平均值为50.65 +/- 2.12 m 100 g-1 min-1，在体积扩张后增加到66.02 +/- 2.00 ml 100 g-1 min-1（P <0.001）。在Wistar大鼠中，在水溶液中的PPF为58.86 +/- 2.33 ml 100 g-1 min-1（与对照动物相比，P <0.01），并且在容量扩张后保持不变。因此，在水肿期间，BEA诱导的乳头坏死导致盐消耗状态和尿浓度缺陷。扩容后，未观察到钠排泄能力紊乱。这些结果与钠排泄调节中的肾单位异质性概念是一致的。组织学病变不能用肾乳头血浆流量减少来解释。
Twenty four hours after i.v. injection of bromoethylamine-hydrobromide (BEA) in rats, a uniform papillary necrosis is observed. The present study investigates the renal functional and the papillary haemodynamics in response to acute volume expansion (12% of body weight) in this model. Renal function studies were performed in hydropenic and volume expanded sham- or BEA-injected rats. In hydropenic normal animals a GFR of 1.97 +/- 0.14 ml/min, an urinary osmolarity (UOsm) of 1 011 +/- 94.5 mOsm/kg and a fractional sodium excretion (FENa) of 0.18 +/- 0.026% were obtained. In contrast, BEA-treated hydropenic animals showed a lower GFR (1.16 +/- 0.14 ml/min), UOsm (469 +/- 30.31 mOsm/kg) and a higher FENa (0.37 +/- 0.06%). In volume expansion a similar UOsm and FENa were obtained in both groups. The papillary plasma flow (PPF) was measured in each of the experimental groups by the albumin accumulation technique. The mean value in hydropenic normal animals was 50.65 +/- 2.12 m 100 g-1 min-1 and increased to 66.02 +/- 2.00 ml 100 g-1 min-1 after volume expansion (P less than 0.001). In BEA rats the PPF was 58.86 +/- 2.33 ml 100 g-1 min-1 in hydropenia (P less than 0.01 vs. control animals) and remained unchanged after volume expansion. Thus, during hydropenia, BEA-induced papillary necrosis results with a salt wasting state and an urinary concentration defect. After volume expansion no disturbance in sodium excretion capacity was observed. These results are compatible with the nephron-heterogeneity concept in the regulation of sodium excretion. The histological lesions cannot be explained by a decreased renal papillary plasma flow.