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全身酸碱平衡紊乱对结肠细胞内pH值和离子转运的影响。

Effect of systemic acid-base disorders on colonic intracellular pH and ion transport.

作者信息

Wagner J D, Kurtin P, Charney A N

出版信息

Am J Physiol. 1985 Jul;249(1 Pt 1):G39-47. doi: 10.1152/ajpgi.1985.249.1.G39.

Abstract

We have previously reported that changes in colonic net Na and Cl absorption correlate with arterial CO2 partial pressure (PCO2) and that changes in colonic net Cl absorption and HCO3 secretion correlate with the plasma HCO3 concentration during the systemic acid-base disorders. To determine whether changes in intracellular pH (pHi) and HCO3 concentration [( HCO3]i) mediate these effects, we measured pHi and calculated [HCO3] in the distal colonic mucosa of anesthetized, mechanically ventilated Sprague-Dawley rats using 5,5-[14C]dimethyloxazolidine-2,4-dione and [3H]inulin. Rats were studied during normocapnia, acute respiratory acidosis and alkalosis, and uncompensated and pH-compensated acute metabolic acidosis and alkalosis. When animals in all groups were considered, there were strong correlations between mucosal pHi and both arterial PCO2 (r = -0.76) and pH (r = 0.82) and between mucosal [HCO3]i and both arterial PCO2 (r = 0.98) and HCO3 concentration (r = 0.77). When we considered the rates of colonic electrolyte transport that characterized these acid-base disorders [A. N. Charney and L. P. Haskell. Am. J. Physiol. 246 (Gastrointest. Liver Physiol. 9): G159-G165, 1984], we found strong correlations between mucosal pHi and net Na absorption (r = -0.86) and between mucosal [HCO3]i and both net Cl absorption (r = 0.98) and net HCO3 secretion (r = 0.83). These findings suggest that the systemic acid-base disorders cause changes in colonic mucosal pHi and [HCO3]i as a consequence of altered arterial PCO2 and HCO3 concentration. In addition, the effects of these disorders on colonic electrolyte transport may be mediated by changes in mucosal pHi and [HCO3]i.

摘要

我们之前报道过,在系统性酸碱紊乱期间,结肠净钠和氯吸收的变化与动脉二氧化碳分压(PCO2)相关,结肠净氯吸收和HCO3分泌的变化与血浆HCO3浓度相关。为了确定细胞内pH(pHi)和HCO3浓度[(HCO3]i)的变化是否介导了这些效应,我们使用5,5-[14C]二甲基恶唑烷-2,4-二酮和[3H]菊粉,在麻醉、机械通气的Sprague-Dawley大鼠的远端结肠黏膜中测量了pHi并计算了[HCO3]。在正常碳酸血症、急性呼吸性酸中毒和碱中毒以及未代偿和pH代偿的急性代谢性酸中毒和碱中毒期间对大鼠进行了研究。当考虑所有组的动物时,黏膜pHi与动脉PCO2(r = -0.76)和pH(r = 0.82)之间以及黏膜[HCO3]i与动脉PCO2(r = 0.98)和HCO3浓度(r = 0.77)之间存在强相关性。当我们考虑表征这些酸碱紊乱的结肠电解质转运速率时[A. N. Charney和L. P. Haskell。《美国生理学杂志》246(胃肠肝脏生理学9):G159 - G165,1984],我们发现黏膜pHi与净钠吸收(r = -0.86)之间以及黏膜[HCO3]i与净氯吸收(r = 0.98)和净HCO3分泌(r = 0.83)之间存在强相关性。这些发现表明,系统性酸碱紊乱由于动脉PCO2和HCO3浓度的改变导致结肠黏膜pHi和[HCO3]i发生变化。此外,这些紊乱对结肠电解质转运的影响可能由黏膜pHi和[HCO3]i的变化介导。

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