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暴露于霍乱毒素的兔回肠中碳酸氢盐分泌的机制。

The mechanism of bicarbonate secretion in rabbit ileum exposed to choleragen.

作者信息

Hubel K A

出版信息

J Clin Invest. 1974 Apr;53(4):964-70. doi: 10.1172/JCI107662.

Abstract

BICARBONATE MAY BE SECRETED INTO THE INTESTINAL LUMEN IN CHOLERA BECAUSE

HCO(3) (-) ions are transported, or because OH(-) ions accumulate and react with dissolved CO(2) to form HCO(3) (-). If HCO(3) (-) ions are transported into the lumen from the interstitial fluid, lumenal P(CO2) should increase (HCO(3) (-) right harpoon over left harpoon OH(-) + CO(2)); if OH(-) accumulates, P(CO2) should diminish. Net movement of H(2)O, and HCO(3) (-), and changes in pH and P(CO2) in lumenal fluid were studied in adjacent segments of rabbit ileum in vivo, one of which was exposed to choleragen. 4 h after exposure, segments were drained and infused with gassed Krebs-Henseleit solution whose P(CO2) exceeded arterial P(CO2). After 45 min, fluid was collected anaerobically from control and cholera segments. Among 13 cholera segments, lumenal P(CO2) diminished by a mean of 8.4 torr and was less than femoral arterial blood in six instances. In the paired control segments, mean P(CO2) increased by 4.4 torr, and was always greater than arterial P(CO2). Dilution could not account for the low P(CO2) in cholera segments because in hypertonic solutions that caused water to move into the lumen, the P(CO2) did not differ from control values obtained with isotonic solutions. The results suggest that OH(-) accumulation (by addition of OH(-) or removal of H(+)) causes HCO(3) (-) secretion in cholera. This does not result from secretion of some other base (e.g., HPO(4) (-)), because HCO(3) (-) accounts for most of the base in the lumenal fluid. The P(CO2) changes suggest that OH(-) reacts with CO(2) at the cell-lumen interface, but reaction at the cell-interstitial fluid interface cannot be excluded.

摘要

在霍乱中,碳酸氢盐可能会分泌到肠腔中,原因如下:HCO(3) (-)离子被转运,或者因为OH(-)离子积累并与溶解的CO(2)反应形成HCO(3) (-)。如果HCO(3) (-)离子从细胞间液转运到肠腔中,肠腔内的P(CO2)应该会增加(HCO(3) (-) ⇌ OH(-) + CO(2));如果OH(-)积累,P(CO2)应该会降低。在体内对兔回肠的相邻节段进行了研究,观察了H(2)O、HCO(3) (-)的净移动以及肠腔内液体的pH和P(CO2)的变化,其中一个节段暴露于霍乱毒素。暴露4小时后,排出节段内的液体,并用P(CO2)超过动脉血P(CO2)的充氧Krebs-Henseleit溶液进行灌注。45分钟后,从对照节段和霍乱节段中厌氧收集液体。在13个霍乱节段中,肠腔内的P(CO2)平均降低了8.4托,有6个节段低于股动脉血中的P(CO2)。在配对的对照节段中,平均P(CO2)增加了4.4托,并且总是高于动脉血P(CO2)。稀释不能解释霍乱节段中P(CO2)较低的原因,因为在导致水进入肠腔的高渗溶液中,P(CO2)与用等渗溶液获得的对照值没有差异。结果表明,OH(-)积累(通过添加OH(-)或去除H(+))导致霍乱中HCO(3) (-)的分泌。这不是由其他一些碱(例如HPO(4) (-))的分泌引起的,因为HCO(3) (-)占肠腔内液体中大部分的碱。P(CO2)的变化表明OH(-)在细胞-肠腔界面与CO(2)反应,但不能排除在细胞-细胞间液界面的反应。

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