The effects of moderate sustained normocapnic hypoxia on tracheal subm
ucosal gland reflex responses were studied. Experiments were performed
in anesthetized, paralyzed, and mechanically ventilated dogs. The cha
nges in the number of secreting glands and volume of secreted fluid in
the subsequent period of time were recorded after 15-30 min of contro
lled ventilation with room air [arterial PO2 (Pa-O2) 86 +/- 3 Torr], h
ypoxic gas mixture (Pa-O2 49 +/- 4 Torr), or 100% O-2 (Pa-O2 339 +/- 3
9 Torr), under isocapnic and isohydric conditions. The hillocks method
was used to quantify the changes in submucosal gland secretion. The c
hanges in secretion 30 s after stimulation of pulmonary C-fiber recept
ors by right atrial injection of capsaicin (10 mu g/kg; n = 10) were m
arkedly lower during moderate hypoxia than in normoxia or hyperoxia. D
ifferences in the number of liquid droplets and the volume of secreted
fluid were statistically significant (P < 0.05 and P < 0.001, respect
ively). Stimulation of airway rapidly adapting receptors by lung defla
tion increased airway secretion; the number of ''hillocks'' and the vo
lume of secreted fluid were lower in hypoxic than in hyperoxic state.
Differences between response curves for the number of glands activated
and secreted volume were statistically significant (P < 0.05 and P <
0.001). The number of glands activated by substance P given locally by
arterial infusion was not affected by the state of oxygenation, but t
he calculated volume of secreted fluid was lower during the hypoxic st
ate than under hyperoxic condition (P = 0.05). When tracheal tension w
as measured (n = 7), hypoxia-potentiated lung deflation induced trache
al constriction (P < 0.05). These findings suggest that prolonged mode
rate hypoxia triggers mechanisms that suppress reflex submucosal gland
responses and potentiate tracheal smooth muscle reflex contraction.