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ALTHOUGH it has long been recognized that defense of pH during acute hypercapnia is dependent on the generation of bicarbonate by body buffers,1 , 2 the quantitative aspects of the response to graded increases in carbon dioxide tension (pCO2) have not been defined in man. The characterization of such a "whole-body titration curve" § should serve the important function of providing a physiologic background against which complex acid–base disturbances in the patient with acute respiratory acidosis might be evaluated.The present study has employed a large environmental chamber to examine the acid–base response of unanesthetized man to progressive elevation of arterial . . .
Brackett et al. (1965) studied this question.