We investigated whether an hypoxia-induced increase in airway resistance me
diated by vagal efferents participates in the increase in end-expiratory lu
ng volume (EELV) observed in hypoxia. We also assessed the contribution of
the end-expiratory activity of the diaphragm (DE) to this phenomenon. There
fore, we measured EELV total lung resistance (RL), dynamic lung compliance
(Cdyn), DE, and minute ventilation (VE) in anesthetized rats during normoxi
a and hypoxia (10% O-2) before (control) and after administration of atropi
ne or saline. In the control group, hypoxia increased EELV, Cdyn, DE, and V
E but slightly decreased RL. These changes were unaffected by saline or atr
opine, except that, in the atropine-treated rats, hypoxia did not change RL
. These results suggest that I)the increase in EELV observed in hypoxia can
not result from an increase in airway resistance; 2)the increased and persi
stent activity of inspiratory muscles during expiration is the most likely
cause of the increase in EELV during hypoxia; and 3) the decrease in RL ind
uced by hypoxia could result from the increase in lung volume including EEL
V.