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金诺芬(SK&F 39162)对犬小肠水和电解质通量的影响:一种可能的致泻机制。

Effect of auranofin (SK&F 39162) on water and electrolyte flux in canine small bowel: a possible diarrheogenic mechanism.

作者信息

Fondacaro J D, Henderson L S, Hardcastle P T, Hardcastle J, Kelleher D K, Ormsbee H S

出版信息

J Rheumatol. 1986 Apr;13(2):288-93.

PMID:3014142
Abstract

Auranofin (AF) a new antiarthritic gold compound effective when administered orally, frequently causes diarrhea with abnormal stool electrolyte content. Studies were designed to determine the mechanism of the diarrhea caused by AF. In perfused canine Thiry-Vella loops, AF caused significant elevations in effluent volume, osmolarity, and sodium concentration and a significant decrease in potassium concentration. In mucosal homogenates of rat small bowel, AF inhibited sodium, potassium ATPase in a concentration dependent manner. AF did not alter canine colonic smooth muscle activity in vitro. We suggest that AF induced diarrhea results from interruption of normal water and electrolyte absorption by inhibition of enterocyte sodium, potassium ATPase activity.

摘要

金诺芬(AF)是一种新型抗关节炎金化合物,口服有效,但常导致腹泻,粪便电解质含量异常。本研究旨在确定AF引起腹泻的机制。在灌注的犬Thiry-Vella肠袢中,AF导致流出液体积、渗透压和钠浓度显著升高,钾浓度显著降低。在大鼠小肠黏膜匀浆中,AF以浓度依赖的方式抑制钠钾ATP酶。AF在体外不改变犬结肠平滑肌活性。我们认为,AF引起的腹泻是由于抑制肠上皮细胞钠钾ATP酶活性,中断了正常的水和电解质吸收所致。

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