Respiratory responses to medullary hydrogen ion changes in cats: different effects of respiratory and metabolic acidoses.

Abstract

The steady-state responses of respiration, measured as integrated phrenic nerve activity, to hypercapnic acidosis of the medullary extracellular fluid (ecf) and to metabolically generated acidosis were compared in paralyzed, vagotomized and glomectomized cats. Ecf hydrogen ion concentration ([H+]) was measured directly by means of a small (2 mm diameter) pH electrode placed on the ventral medulla. Changes of medullary ecf [H+] were linearly related to changes of end-tidal PCO2 [partial pressure of CO2], both before (r = 0.999) and after (r = 0.996) the development of metabolic acidosis. There was a curvilinear relation between hypercapnic ecf [H+] changes and the respiratory response that reflects progressive saturation of a central neural pathway between the chemoreceptors and the respiratory controller. This relation was similar in form both before and after development of metabolic acidosis. When acidosis of metabolic origin was present, apnea occurred with only small decreases of CO2 despite a high [H+]. The respiratory responses to the same ecf [H+] change were only .apprx. 1/2 as large when they were generated metabolically as when they were generated by raising PCO2. Both exogenously induced metabolic acidosis (HCl infusion) and endogenous acidosis yielded similar results. The ecf [H+] does not represent the unique stimulus to the central chemoreceptors.