Am. J. Respir. Crit. Care Med.,
Volume 158, Number 3, September 1998, 742-748
Control of Ventilation during Lung Volume Changes
and Permissive Hypercapnia in Dogs
MICHAEL L.
CARL,
EDWARD S.
SCHELEGLE,
STEVEN B.
HOLLSTIEN,
and
JERRY F.
GREEN
Emergency Department, Kaiser Permanente Hospital, South Sacramento and Division of Emergency Medicine, University of California,
Davis Medical Center, Sacramento; Department of Anatomy, Physiology and Cell Biology, School of Veterinary Medicine,
and Department of Human Physiology, School of Medicine, University of California, Davis, Davis, California
We investigated the effect changes in end-expiratory lung volume (EEVL) had on the response to progressive hypercapnia (CO2-response curve) in eight open-chest, anesthetized dogs, in order to clarify the role that vagal lung mechanoreceptors have in altered respiratory drive during permissive hypercapnia. The dogs were ventilated using a positive-pressure ventilator driven by phrenic neural activity. Systemic arterial CO2 tension (PaCO2) was elevated by increasing the fraction of CO2 delivered to
the ventilator. EEVL was altered from approximated functional residual capacity ("FRC") to 1.5 and
0.5 "FRC" by changing positive end-expiratory pressure. Although the tidal volume (VT)-PaCO2 and inspiratory time (TI)-PaCO2 relationships were not affected, decreasing 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
minute ventilation (
I) and frequency (f ), and a significant (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 receptors (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
the apneic threshold, which we attribute to an inhibitory effect on central drive caused by increased
PSR activity.
