CONTROL OF VENTILATION DURING LUNG-VOLUME CHANGES AND PERMISSIVE HYPERCAPNIA IN DOGS

We investigated the effect changes in end-expiratory lung volume (EEVL ) had on the response to progressive hypercapnia (CO,response curve) i n eight open-chest, anesthetized dogs, in order to clarify the role th at vagal lung mechanoreceptors have in altered respiratory drive durin g permissive hypercapnia. The dogs were ventilated using a positive-pr essure ventilator driven by phrenic neural activity. Systemic arterial CO2 tension (Pa-CO2) was elevated by increasing the fraction of CO2 d elivered to the ventilator. EEVL was altered from approximated functio nal residual capacity (''FRC'') to 1.5 and 0.5 ''FRC'' by changing pos itive end-expiratory pressure. Although the tidal volume (VT)-Pa-CO2 a nd inspiratory time (TI)-Pa-CO2 relationships were not affected, decre asing EEVL from 1.5 ''FRC'' to ''FRC'' and then to 0.5 ''FRC'' caused a significant (p < 0.01) upward shift in the CO2-response curves for m inute ventilation ((V) over dot I) and frequency (f), and a significan t (p < 0.01) downward shift in the CO2- response curve for expiratory time (TE). We conclude that these shifts were explained by a decrease in the inhibitory activity of slowly adapting pulmonary stretch recept ors (PSRs) as EEVL was lowered. In addition, increases in EEVL from 0. 5 ''FRC'' to 1.5 ''FRC'' caused a significant (p < 0.05) increase in t he apneic threshold, which we attribute to an inhibitory effect on cen tral drive caused by increased PSR activity.