The present study evaluated the mechanisms by which upper airway (UAW)
-dilating muscle contraction, elicited by hypoglossus nerve (HGN) stim
ulation, improved UAW patency. Pressure-flow (P-V) relationships of th
e isolated UAW as well as the negative intraluminal pressures required
to cause UAW collapse were assessed before and during electrical stim
ulation of the HGN in 8 anesthetized, ventilated dogs. Sectioning of t
he HGN shifted the P-V relationship to the left, while electrical stim
ulation resulted in a substantial shift of the curve to the right, ind
icating UAW dilatation. UAW resistance decreased from 9.0 +/- 1.5 to 0
.3 +/- 0.1 cm H2O . l(-1). s during HGN stimulation (p < 0.01). The ma
gnitude of negative intraluminal pressure at which UAW collapse occurr
ed (the critical pressure) increased from -2.7 +/- 0.7 to -13.2 +/- 2.
1 cm H2O (p < 0.002). The increase in UAW conductance and stability ra
ised the maximal flow which could be sustained without collapse from 0
.28 +/- 0.07 to 2.07 +/- 0.35 Vs during HGN stimulation (p < 0.001). T
hese findings indicate that in the anesthetized dog, UAW muscle contra
ction improves UAW patency both by dilating the UAW and by stiffening
its walls.