The present study was undertaken to gain further insight into the mechanism
s responsible for the sustained active expiratory upper airway closure prev
iously observed during high-permeability pulmonary edema in lambs. The expe
riments were conducted in nonsedated lambs, in which airflow and thyroaryte
noid and inferior pharyngeal constrictor muscle electromyographic activity
were recorded. We first studied the consequences of hemodynamic pulmonary e
dema (induced by impeding pulmonary venous return) on upper airway dynamics
in five lambs; under this condition, a sustained expiratory upper airway c
losure consistently appeared. We then tested whether expiratory upper airwa
y closure was related to vagal afferent activity from bronchopulmonary rece
ptors. Five bivagotomized lambs underwent high-permeability pulmonary edema
: no sustained expiratory upper airway closure was observed. Finally, we st
udied whether a sustained decrease in lung volume induced a sustained expir
atory upper airway closure. Five lambs underwent a 250-ml pleural infusion:
no sustained expiratory upper airway closure was observed. We conclude tha
t 1) the sustained expiratory upper airway closure observed during pulmonar
y edema in nonsedated lambs is related to stimulation of vagal afferents by
an increase in lung water and 2) a decrease in lung volume does not seem t
o be the causal factor.