Changes in intrapulmonary chemoreceptor discharge in response to the adjustment of respiratory pattern during hyperventilation in domestic fowl.
It has been suggested that avian vagal intrapulmonary CO2-sensitive receptors (i.p.c.) may be capable of monitoring the rate and extent of CO2 wash-out from the lung during spontaneous breathing. The purpose of this study was to record i.p.c. discharge activity in spontaneously breathing domestic fowl when minute volume (VI) was elevated from resting levels. This was accomplished by administration of almitrine (2 mg X kg-1 I.V.), a respiratory stimulant drug that has been shown to have a specific long-lasting stimulatory action on carotid body chemoreceptors. Unanaesthetized decerebrate fowl were tracheotomized and single-unit activity was recorded from sixteen vagal i.p.c. When ventilation was elevated 2.2-fold by almitrine (initially by increases in tidal volume (VT)) i.p.c. discharge was increased in both inspiration and expiration, and the delay period before the onset of i.p.c. discharge in inspiration was markedly shortened. Within 5-10 min after the administration of almitrine, the breathing pattern changed to one of rapid, shallow breathing, although the 2.2-fold elevation of the rate of gas flow through the parabronchi (V) and mean inspiratory flow rate (VT/TI) were maintained. The i.p.c. continued to fire phasically, with peaks of discharge in both inspiration and expiration, though there were fewer spikes per breath and mean inspiratory peak discharge rate returned to control (eupnoeic) levels. It is concluded that i.p.c. discharge is increased when VI is elevated in the spontaneously breathing fowl and that the pattern of discharge is dependent on the pattern of breathing. I.p.c. show high dynamic sensitivity to changes in the PCO2 of their microenvironment and it is possible to explain the changes in discharge pattern observed in terms of the PCO2 changes in the lungs and air sacs. These results support proposals that the pattern of breathing is to some extent dependent upon the intensity and timing of i.p.c. activity.
D015765:Almitrine; D000818:Animals; D002245:Carbon Dioxide / Q000378:metabolism; D002344:Carotid Body / Q000502:physiology; D002628:Chemoreceptor Cells / Q000187:drug effects / Q000502:physiology*; D002645:Chickens; D004594:Electrophysiology; D005260:Female; D006985:Hyperventilation / Q000139:chemically induced / Q000503:physiopathology*; D008168:Lung / Q000187:drug effects / Q000503:physiopathology*; D010879:Piperazines / Q000494:pharmacology; D012119:Respiration / Q000187:drug effects; D013990:Tidal Volume
D010879:Piperazines; D002245:Carbon Dioxide; D015765:Almitrine