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α-萘基异硫氰酸酯诱导的实验性肝内胆管炎中的多尿

Polyuria in experimental intrahepatic cholangitis induced by alpha-naphthyl-isothiocyanate.

作者信息

Tur-Kaspa R, Adler R, Popovtzer M M, Eliakim M

出版信息

Eur J Clin Invest. 1983 Feb;13(1):19-24. doi: 10.1111/j.1365-2362.1983.tb00059.x.

DOI:10.1111/j.1365-2362.1983.tb00059.x
PMID:6409620
Abstract

Alpha-naphthyl-isothiocyanate (ANIT)-induced intrahepatic cholangitis was associated with significant polyuria in rats. The urine output in the experimental rats was about two and a half to four fold higher than that in the controls. The polyuria was accompanied by polydypsia and disappeared when water intake was limited and controlled. The glomerular filtration rate and renal histology remained intact. Dilution and concentration capacities were preserved and the response to exogenous anti-diuretic hormone was intact. Following water deprivation, the water and electrolyte contents of the renal medulla and papilla were similar in both experimental and control rats. The excretion of a salt-load in ANIT-treated rats was delayed. It is concluded that the polyuria in ANIT-treated rats is secondary to polydypsia. The finding of preserved dilution and concentration capacities in this experimental model contrasts to that in other experimental models of hepatobiliary disease.

摘要

α-萘基异硫氰酸酯(ANIT)诱导的肝内胆管炎与大鼠显著的多尿有关。实验大鼠的尿量比对照组高约二点五至四倍。多尿伴有烦渴,当水摄入量受到限制和控制时多尿消失。肾小球滤过率和肾脏组织学保持完整。稀释和浓缩能力得以保留,对外源性抗利尿激素的反应也正常。禁水后,实验大鼠和对照大鼠肾髓质和乳头的水和电解质含量相似。ANIT处理的大鼠对盐负荷的排泄延迟。得出的结论是,ANIT处理的大鼠多尿是烦渴的继发症状。在该实验模型中发现的保留的稀释和浓缩能力与其他肝胆疾病实验模型中的情况形成对比。

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