The Mechanism of Bicarbonate Secretion in Rabbit Ileum Exposed to Choleragen

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Abstract

Bicarbonate may be secreted into the intestinal lumen in cholera because: HCO3− ions are transported, or because OH− ions accumulate and react with dissolved CO2 to form HCO3−. If HCO3− ions are transported into the lumen from the interstitial fluid, lumenal PCO2 should increase (HCO3− ⇌ OH− + CO2); if OH− accumulates, PCO2 should diminish. Net movement of H2O, and HCO3−, and changes in pH and PCO2 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 PCO2 exceeded arterial PCO2. After 45 min, fluid was collected anaerobically from control and cholera segments. Among 13 cholera segments, lumenal PCO2 diminished by a mean of 8.4 torr and was less than femoral arterial blood in six instances. In the paired control segments, mean PCO2 increased by 4.4 torr, and was always greater than arterial PCO2. Dilution could not account for the low PCO2 in cholera segments because in hypertonic solutions that caused water to move into the lumen, the PCO2 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 HCO3− secretion in cholera. This does not result from secretion of some other base (e.g., HPO4−), because HCO3− accounts for most of the base in the lumenal fluid. The PCO2 changes suggest that OH− reacts with CO2 at the cell-lumen interface, but reaction at the cell-interstitial fluid interface cannot be excluded.

Authors

Kenneth A. Hubel