Ventilatory response to inspired CO2 in normal and carotid body-denervated ponies.

The purpose of these studies was to gain insight into mechanisms regulating pulmonary ventilation (VE), arterial CO2 partial pressure (PaCO2), and arterial pH (pHa) in ponies when inspired CO2 partial pressure (PICO2) is above normal. Ponies were studied four times daily each weekday for 2 wk in an environmental chamber. Each study consisted of a 15-min control period (PICO2 = 0.7 Torr) followed by a 15- to 30-min experimental period during which PICO2 in the chamber was 0.7, 7, 14, 21, 28, or 42 Torr (PIO2 = 147 Torr throughout). Between 11 and 15 min of each period, four 3-ml samples of arterial blood were drawn, each over 45 s. In 12 normal ponies, elevation of PICO2 to 7 Torr caused PaCO2 to increase approximately 0.4 Torr (P less than 0.01) and pHa to decrease approximately 0.003 (P less than 0.02) relative to control. The hypercapnia and acidosis increased progressively as PICO2 was increased in 7- to 14-Torr increments to 42 Torr (P less than 0.02). Accordingly, the hyperpnea in these ponies during CO2 inhalation could have been mediated by carotid and intracranial chemoreceptors. One month after carotid body denervation (CBD) in nine ponies, PaCO2 during control conditions was 6 Torr above normal, but during CO2 inhalation, PaCO2 changed less from control than during CO2 inhalation before CBD (P less than 0.01). The delta VE/ delta PaCO2 near eupneic PaCO2 appeared to be above normal 1 mo after CBD (P less than 0.01). The mechanism of this increase was not discernible from our data. Finally, our data indicated that the magnitude of the hypercapnia and acidosis during CO2 inhalation was inversely related to PaCO2 and breathing frequency during control conditions.