Pulmonary afferent control of breathing as end-expiratory lung volume decreases

We studied reflex changes in breathing elicited by graded reductions in end-expiratory lung volume (EEV(L)) and the vagal nerves responsible. The chests of nine dogs anesthetized with α-chloralose were opened, and the lungs were ventilated by a phrenic nerve-driven servo-respirator. The immediate effects of a 50% reduction in end-expiratory transpulmonary pressure (EEPtp) from control (EEVL equivalent to functional residual capacity) were to significantly increase both tidal volume (VT) and breathing frequency (f) from 0.402 ± 0.101 to 0.453 ± 0.091 liter (mean ± SD) and 11.8 ± 5.4 to 15.7 ± 6.4 breaths/min, respectively (P < 0.05). Further reductions in EEPtp to 0 cmH₂O did not change VT but augmented f to 19.6 ± 6.6 breaths/min (P < 0.05). The increase in f as EEVL decreased was due entirely to a reduction in expiratory time. Vagotomy abolished these reflexes. By 90 s after reduction in EEVL, arterial PCO₂ fell significantly and VT returned to or below control values. We therefore repeated these experiments in five dogs whose blood gases were controlled by cardiopulmonary bypass. There were no secondary changes in VT and by 90 s breathing pattern could be characterized as rapid and deep. In another eight dogs submitted to the same collapse protocol, we recorded action potentials from all known categories of pulmonary vagal afferents. These studies demonstrated that the changes in breathing pattern induced by a 50% reduction in EEPtp were due to a withdrawal of slowly adapting stretch receptor activity; however, continued increases in f as EEVL was reduced further were due to increases in rapidly adapting stretch receptor activity. The only effect on breathing pattern elicited by rapidly adapting stretch receptors was a decrease in expiratory time.