Changes in strength of lung inflation reflex during prolonged inflation.
Recovery from respiratory inhibition produced by the lung inflation reflex was studied in anesthetized dogs, paralyzed and ventilated with a respiratory pump. During constant ventilation the lungs were periodically inflated using positive end-expiratory pressure, while the respiratory motor output was monitored in the phrenic nerve. Inhibition of the phrenic discharge was followed by gradual recovery throughout 8-min inflation periods despite constant blood gases. Recording afferent potentials in a vagus nerve indicated that adaptation of pulmonary stretch receptors contributed to the initial recovery of the phrenic discharge, but this recovery continued after the receptor discharge had stabilized. The phrenic discharge also recovered after initial inhibition in two situations which avoided stretch receptor adaptation: a) when the stretch receptor discharge from the separate lungs was alternated in an overlapping manner by asynchronous pulmonary ventilation, and b) during continuous electrical stimulation of a vagus nerve. Phrenic activity was temporarily increased above its control value after periods of lung inflation, asynchronous ventilation and vagal stimulation. It is concluded that the lung inflation reflex gradually attenuates during prolonged stimulation due to both stretch receptor adaptation and changes within the central pathways.
D000222:Adaptation, Physiological; D000818:Animals; D004285:Dogs; D004558:Electric Stimulation; D006185:Habituation, Psychophysiologic; D008168:Lung / Q000294:innervation*; D009433:Neural Inhibition; D009475:Neurons, Afferent / Q000502:physiology; D010791:Phrenic Nerve / Q000502:physiology; D011175:Positive-Pressure Respiration; D011661:Pulmonary Stretch Receptors / Q000502:physiology; D012018:Reflex; D012119:Respiration; D009435:Synaptic Transmission; D013997:Time Factors; D014630:Vagus Nerve / Q000502:physiology