It is generally agreed that in metabolic acidosis respiration is stimulated, with consequent reduc- tion of alveolar and arterial CO2 pressure, Pco2; in metabolic alkalosis, however, there has been disagreement as to whether or not there is a cor- responding respiratory inhibition, with elevation of Pco2.Evidence that such inhibition does oc- cur has been presented in several reports (1-4); on the other hand, some investigators have found no significant change in Pco2 (5).Opportunity for the collection of further evidence on this ques- tion was afforded by a series of studies on the ef- fects of acute metabolic alkalosis induced in hu- man subjects by the infusion of hypertonic sodium bicarbonate solution, approximately 2.3 mEq.per kilogram of body weight.The first paper of this series (6) described the ionic transfers as observed in arterial or cutaneous blood, and calculated for extracellular and other body fluid compartments, including the volume of distribution of the excess sodium bicarbonate.The plasma acid-base data from these experiments readily permit the calcu- lation of arterial Pco2, before, during, and for two hours following the infusion.We consider the changes in calculated arterial Pco2 to repre- sent the most reliable index of respiratory changes, because this sampling method produced the least disturbance to respiration.However, we are also reporting in this, the second paper of the series, results of additional experiments in which alveolar Pco2, total pulmonary ventilation, and respiratory
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Singer et al. (1956) studied this question.