Ventilatory response to the PCO2 profile in chicken lungs.

We investigated the influence of intrapulmonary chemoreceptors (IPC) on ventilatory movements in anesthetized chickens when PCO2 profiles along the parabronchi were changed. In all experiments the right lung was denervated, both lungs unidirectionally ventilated, and PaCO2 kept constant. In series 1 (7 birds), gas flow and the PCO2 profile in the left lung were reversed. PaCO2, PECO2 and ventilatory movements did not change. In Series 2 (4 birds), PCO2 in caudal regions of the innervated lung was elevated by increasing gas flow and P1CO2 from 0 to 21 Torr. Ventilatory movements did not change. In Series 3 (4 birds), either lung was over-ventilated with 7 or 49 Torr P1CO2, alternating the gases between lungs every 100 sec. Ventilatory movements changes with P1CO2 but much less than predicted from P1CO2 effects in the non-perfused, innervated lung. From the longitudinal distribution of IPC and PCO2 profiles in the lung we predicted moderate to large changes in ventilatory movements in all series. The discrepancy between predicted and observed results in Series 1 and 2 indicates that IPC in caudal regions of the lung have little effect on ventilation under the conditions examined. In Series 3, observed ventilatory movements were less sensitive to P1CO2 than predicted, indicating that IPC sense a different PCO2 than the PCO2 profile in the parabronchial lumen and that IPC have a significant sensitivity to pulmonary blood PCO2.

Chicken intrapulmonary chemoreceptor discharge frequency reduced by increasing rate of repetitive PCO2 changes.

We have recently reported that repetitive changes of PCO2 given to innervated non-perfused chicken lungs reflexly inhibit respiratory efforts. The degree of respiratory inhibition is rate-dependent, decreasing as repetition rate is increased to 3 . 2 Hz (Barker, Burger & Nye, 1981) to nearly that expected from the average PCO2 of the two levels given. Intrapulmonary chemoreceptors (i.p.c.s), whose discharge frequencies are inversely related to PCO2, are presumably responsible for these effects. Here we report the activity of twenty single i.p.c.s in the left, non-perfused lungs of twelve thoractomized cockerels as PCO2 of the gas ventilating those lungs was repetively changed between 7 and 27 or 7 and 40 torr. Maximal discharge rates of individual receptors after a PCO2 decrease were related to the location of receptors within the gas exchange region. From 0 . 2 to 1 . 6 Hz both average and maximal discharge frequencies decreased. The inhibition of discharge in this range was greater than that predicted by the steady-state relationship between reflex responses and receptor discharge, suggesting that the reflex effects of i.p.c. discharge are not a simple function of the mean discharge frequency of all i.p.c.s. Either average i.p.c. discharge frequency per PCO2 cycle over-estimates their respiratory reflex inhibition or only the less rate-sensitive i.p.c.s, those in the middle of the gas exchange region, may dominate this rate-dependent respiratory reflex.

Respiratory inhibition from chicken intrapulmonary chemoreceptors reduced by increasing rate of repetitive PCO2 changes.

There is no functional residual capacity in the avian lung, so during inspiration the PCO2 of the gas entering the exchange region abruptly changes from its maximum, the dead space PCO2, to its minimum, the inspired PCO2. Dynamic responses of intrapulmonary chemoreceptors (i.p.c.s) to positive and negative going steps in PCO2 are asymmetrical and have maxima occurring at times comparable to inspiratory duration. Thus, the respiratory inhibition that i.p.c.s produce could depend on respiratory frequency. We tested this hypothesis by changing intrapulmonary PCO2 repetitively between 7 and 42 torr in the non-perfused left lungs of eight unidirectionally ventilated thoracotomized chickens. Right intrapulmonary and arterial PCO2 were kept constant. Respiratory movements were calibrated in terms of steady state intrapulmonary PCO2 levels. At PCO2 repetition rates comparable to normal respiratory frequency, respiratory movements were equal to those expected for an intrapulmonary PCO2 2--3 torr lower than the average of the two PCO2 levels used. This difference increased linearly as the logarithm of the repetition rate decreased. We conclude that respiratory inhibition by i.p.c.s is inversely related to respiratory rate as well as to average intrapulmonary PCO2 levels. Because respiratory frequency itself is negatively related to i.p.c. discharge frequency, i.p.c.s may provide control over respiratory frequency even if average PCO2 levels do not change.