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

Abstract

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.

Effects of hypercapnic hyperpnea on recovery from isoflurane or sevoflurane anesthesia in horses

“…Our original hypothesis predicted that anesthetic elimination would be faster with sevoflurane than isoflurane, as a result of the lower blood solubility for the former (Bergadano et al. 2003), and faster with CO 2 insufflation than without, as a result of increased stimulation of alveolar minute ventilation (Klein et al. 1982).…”

“…In addition, PvCO 2 for horses insufflated with 10% CO 2 was lower than PCO 2 of the insufflated gas, thereby proving that insufflated gases were considerably diluted with ambient air during inspiration. The effect of CO 2 on anesthetic washout was greater for isoflurane than for sevoflurane; pharmacokinetic effects were presumably due to increased alveolar minute ventilation (Klein et al. 1982; Vesely et al.…”

Breath-to-breath hypercapnic response in neonatal rats: temperature dependency of the chemoreflexes and potential implications for breathing stability

“…Most studies have used relatively long periods of gas exposure during which the ventilatory response to CO 2 is not only influenced heavily by secondary effects (e.g., changes in T B ), but also represents the combined inputs from both peripheral and central chemoreceptors to the respiratory controller, making it difficult to assess the independent contribution of the peripheral chemoreflex. Indeed, the stability of eupneic ventilation V E in newborns might rely more heavily on carotid body inputs to the respiratory controller; the carotid bodies have been shown to have a well-developed CO 2 response at birth (7,9,11,13) and (at least in adults) have been shown to be important determinants of eupneic breathing and arterial PCO 2 homeostasis (4,20,27,36). Few studies, however, have attempted to characterize the carotid body responsiveness to CO 2 in intact, unanesthetized, newborn rodents.…”

The apneic threshold during non-REM sleep in dogs: sensitivity of carotid body vs. central chemoreceptors

“…However, both of these types of studies have major limitations, which preclude generalization of these findings to the intact sleeping animal or human. For example, carotid body denervation is known to markedly reduce baseline eupneic ventilation and cause CO 2 retention (13,33), to upregulate aortic chemoreceptors (4,20,29), to reduce the CO 2 responsiveness of central chemoreceptors (16,25,38), to alter the response of central chemoreceptors to focal acidosis (18), and to decrease cytochrome oxidase activity in the pre-Bötzinger complex of neonatal rats (21), and it can alter responses to systemic hypoxia and cyanide in CO 2 -sensitive neurons in the retrotrapezoid nucleus (38).…”