实验性范科尼综合征中钠肠道转运及黏膜（钠-钾）-ATP酶的抑制作用
Inhibition of sodium intestinal transport and mucosal (Na+-K+)-ATPase in experimental Fanconi syndrome.
作者信息
Wapnir R A, Exeni R A, McVicar M, De Rosas R J, Lifshitz F
出版信息
Proc Soc Exp Biol Med. 1975 Nov;150(2):517-20. doi: 10.3181/00379727-150-39068.
The administration of 1.5 or 9.0 mmoles/kg ip of maleate to rats induced, in addition to renal alterations similar to those occurring in the Fanconi syndrome, a decline in the intestinal mucosa (Na+-K+)-ATPase with a simultaneous decrease in sodium intestinal transport and an increase in potassium absorption. Further differences in the behavior of the two electrolytes were observed when the concentration of sodium in the perfusates was altered. No changes occurred in amino acid or glucose transport in experimental animals.
给大鼠腹腔注射1.5或9.0毫摩尔/千克马来酸盐，除了引起类似于范科尼综合征中出现的肾脏改变外，还导致肠黏膜（钠 - 钾）-ATP酶活性下降，同时肠道钠转运减少，钾吸收增加。当改变灌注液中钠的浓度时，观察到两种电解质行为的进一步差异。实验动物的氨基酸或葡萄糖转运未发生变化。
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