ROLE OF THE ARTERIAL CHEMORECEPTORS IN VENTILATORY AND CIRCULATORY ADJUSTMENTS TO HYPOXIA IN AWAKE PEKIN DUCKS

Awake male Pekin ducks were studied either after chronic bilateral carotid body denervation (CBD), or intact or sham-operated (control). At neutral ambient temperature, they were subjected to acute, prolonged or chronic hypoxia (30 min, 3 h and 15 d, respectively) at an inspired(Formula presented.) of 90 or 98 Torr. Resting ventilation, pulmonary gas exchange, arterial blood gases and pH, and ventilatory responses to brief O2 inhalation were measured. In ducks in prolonged hypoxia, mixed venous blood gases and O2 convection by blood were also measured in steady state conditions. Chronic bilateral denervation of the carotid bodies abolished the arterial chemoreflex drive of breathing, as judged from the lack of ventilatory response to transient O2-inhalation. CBD birds retained a normal oxygen consumption in hypoxia and normoxia. In normoxia, carotid body denervation resulted in hypoventilation, hypercapnia and respiratory acidosis; O2 extraction from air ((Formula presented.)) increased in CBD ducks, but O2 convection by blood was not affected. In acute, prolonged and chronic hypoxia, control ducks hyperventilated with consequent hypocapnia and increase of arterial(Formula presented.); CBD ducks did not hyperventilate, remained hypercapnic and were very hypoxic. The greater circulatory O2-conductance observed in ducks in prolonged hypoxia was due to an increased capacitance coefficient of blood for oxygen ((Formula presented.)) in control birds, and to increases in both(Formula presented.) and cardiac output (b) in CBD ducks. It is concluded that, in awake Pekin ducks, integrity of the arterial chemoreflex of breathing is essential for determining the eupneic level of ventilation in normoxia as well as in hypoxia. The drive, being entirely responsible for the ventilatory response to hypoxia, minimizes the degree of hypoxemia, and spares the convective circulatory requirement from increasing under prolonged hypoxic exposure. © 1979, Springer-Verlag. All rights reserved.