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Acute and steady-state responses to hypercapnia of respiratory output, measured as integrated phrenic nerve activity, and medullary extracellular fluid (e.c.f.) pH, measured directly, were determined in paralysed, vagotomized and glomectomized cats. Medullary e.c.f. pH responds within seconds to an acute change of alveolar and arterial PCO2. The respiratory response closely and inversely matches the e.c.f. pH change, but not the cerebrospinal fluid pH change. The medullary e.c.f. pH change following a rapid step-change in end-tidal PCO2 requires at least 5 min for a new steady state to be achieved. Steady-state studies in twenty-six cats show: (a) that the respiratory response to progressive hypercapnic stimulation of the central chemoreceptors is curvilinear (Eldridge, Gill-Kumar & Millhorn, 1981), (b) that the relationship between increasing end-tidal PCO2 and medullary hydrogen ion concentration [(H+]) or changes of pH is linear (r = 0.995); a doubling of PCO2 causes 0.260 units pH change, (c) there is a curvilinear relationship between e.c.f. [H+] and the respiratory response that is the same as that found with CO2. We conclude that medullary e.c.f. pH measured by means of a surface electrode accurately reflects the CO2-induced [H+] stimulus to respiration. The decreasing respiratory responses to identical changes of central chemoreceptor input are due to progressive neuronal saturation of a central pathway between the chemoreceptors and the respiratory controller.

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