THE KINETICS OF BICARBONATE REABSORPTION DURING ACUTE RESPIRATORY ACIDOSIS*

It is well-known that acute elevation of blood pCO2 is accompanied by a rise in the renal reabsorption of bicarbonate (1-3). The exact mechanism through which this occurs has not been established, but it is thought to result from accelerated tubular hydrogen secretion due either to the lowering of c...

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Bibliographic Details
Main Authors: William B, T Adrien Falbriard, Guy Lemieux
Other Authors: The Pennsylvania State University CiteSeerX Archives
Format: Text
Language:English
Published: 1958
Subjects:
Online Access:http://citeseerx.ist.psu.edu/viewdoc/summary?doi=10.1.1.429.6863
http://www.jci.org/articles/view/103876/version/1/pdf/render/
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Summary:It is well-known that acute elevation of blood pCO2 is accompanied by a rise in the renal reabsorption of bicarbonate (1-3). The exact mechanism through which this occurs has not been established, but it is thought to result from accelerated tubular hydrogen secretion due either to the lowering of cellular pH or to an increased formation of carbonic acid. The present experiments were undertaken in an attempt to define further the nature of the reabsorptive process during acute respiratory acidosis. The data demonstrate that during an acute sustained increase of carbon dioxide tension, progressive elevation of plasma bicarbonate concentration was accompanied by a curvilinear increase in the rate of bicarbonate reabsorption. The relationship between plasma bicarbonate concentration and the rate of reabsorption was found, by means of the double reciprocal plot, to take the form + The possible significance of this finding has been considered. MATERIALS AND METHODS Twelve experiments were performed on female mongrel dogs anesthetized with sodium pentobarbital. An endotracheal tube fitted with an inflatable balloon was introduced into the trachea and connected either to a calibrated volume displacement ventilator (Etsten Ventilator) (4) or to a Mine Safety "Pneophore. " Respiratory movements were inhibited by the administration of gallamine triethiodide (Flaxedil®) so that respiratory exchange could be controlled by the ventilator. Blood pCO2 was increased to values of approximately 90 to 100 mm. Hg by having the animal breathe a mixture of 9 per cent CO2 and 91 per cent oxygen. This tension was then kept as constant