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Departments of 1 Pediatrics, 3 Medicine, and 4 Anatomy, Rainbow Babies and Children's Hospital, School of Medicine, Case Western Reserve University; and 2 Department of Pathology, Cleveland Clinic Foundation, Cleveland, Ohio 44106
We sought to
define the effects of maturation and hyperoxic stress on nitric oxide
(NO)-induced modulation of bronchopulmonary responses to stimulation of
vagal preganglionic nerve fibers. Experiments were performed on
decerebrate, paralyzed, and ventilated rat pups at 6-7 days
(n = 21) and 13-15 days of age (n = 23) breathing room air and on rat pups 13-15 days of age
(n = 19) after exposure to hyperoxia (
95% inspired
O2 fraction for 4-6 days). Total lung resistance
(RL) and lung elastance (EL) were measured by
body plethysmograph. Vagal stimulation and release of acetylcholine caused a frequency-dependent increase in RL and
EL in all animals. The RL response was
significantly potentiated in normoxic animals by prior blockade of
nitric oxide synthase (NOS) (P < 0.05). Hyperoxic exposure increased responses of RL to vagal stimulation
(P < 0.05); however, after hyperoxic exposure, the
potentiation of contractile responses by NOS blockade was abolished.
The response of EL was potentiated by NOS blockade in the
13- to 15-day-old animals after both normoxic and hyperoxic exposure
(P < 0.01). Morphometry revealed no effect of
hyperoxic exposure on airway smooth muscle thickness. We conclude that
NO released by stimulation of vagal preganglionic fibers modulates
bronchopulmonary contractile responses to endogenously released
acetylcholine in rat pups. Loss of this modulatory effect of NO could
contribute to airway hyperreactivity after prolonged hyperoxic
exposure, as may occur in bronchopulmonary dysplasia.
airway smooth muscle; development
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