Hyperoxic hyperventilation in carotid-deafferented cats.
Ventilation when breathing air and during exposure to hyperoxia (PAO2 equal to 400-450 mm Hg) was studied in unanesthetized cats before and after carotid sinus nerve section (chemo-deafferentation). Chemo-deafferentation resulted in lowered values of measured ventilation, tidal volume, and respiratory frequency, during air breathing PACO2 increased by an average of 7.9 mm Hg. In intact animals, ventilation after 10 minutes of exposure to hyperoxia was similar in magnitude and pattern to that measured during air breathing. Exposure of chemo-deafferented animals to hyperoxia resulted in an increased ventilation, due entirely to augmented tidal volume. Increased ventilation was accompanied by a decrease in PACO2. This response to hyperoxia developed gradually duringa 3-4-minute period, the rise in ventilation and fall in PACO2 invariably stabilizing by 5 minutes. It is concluded that carotid body chemoreceptor activity is essential for the maintenance of normal values of ventilation and PACO2 in unanesthetized cats. In addition, central mechanisms responsible for tidal volume production may, in the absence of carotid body afferent input, be depressed by the PO2 characteristic of normal arterial blood. The significance of these findings to the chemical control of breathing is discussed.
D000388:Air; D000818:Animals; D002245:Carbon Dioxide / Q000097:blood; D002344:Carotid Body / Q000502:physiology*; D002346:Carotid Sinus / Q000294:innervation*; D002415:Cats; D002628:Chemoreceptor Cells / Q000502:physiology; D003714:Denervation; D006985:Hyperventilation / Q000097:blood / Q000503:physiopathology*; D000860:Hypoxia / Q000097:blood / Q000503:physiopathology*; D009474:Neurons / Q000502:physiology*; D009475:Neurons, Afferent / Q000502:physiology*; D012119:Respiration; D013147:Spirometry; D013990:Tidal Volume
D002245:Carbon Dioxide