Abstract

In pentobarbitone anesthetized cats, raising body temperature from 37 to 40-degrees-C by external heat increased respiratory frequency, tidal volume, frequency of spontaneous gasps and mean inspiratory flow. It reduced end-tidal CO2 pressure, together with inspiratory and expiratory durations. After bilateral section of the carotid nerves, raising body temperature still induced hyperventilation, but the increase in gasp frequency was less pronounced and no significant change in tidal volume was observed. In comparison to steady ventilatory values in the intact condition, significant reductions in tidal volume at 38-degrees-C and in gasp frequency at 37, 39 and 40-degrees-C were observed after bilateral carotid neurotomy. Brief hyperoxic tests induced transient decreases in tidal volume and increases in end-tidal CO2 pressure which were significantly larger at 40-degrees-C than at 37-degrees-C. These changes disappeared after bilateral carotid neurotomy. Anesthetic block of both carotid nerves produced transient reductions in tidal volume at any given temperature. We conclude that carotid body afferents contribute to the hyperventilation evoked by hyperthermia. After their interruption, such contribution is replaceable from other thermal afferents.