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1 Department of Pediatrics, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106-6010; and 2 Department of Physiology and Biophysics, Specialized Neuroscience Research Program, Howard University College of Medicine, Washington, DC 20059
The role of
endogenous nitric oxide (NO) in modulating the excitatory response of
distal airways to vagal stimulation is unknown. In decerebrate,
ventilated, open-chest piglets aged 3-10 days, lung resistance
(RL) was partitioned into tissue resistance (Rti) and
airway resistance (Raw) by using alveolar capsules. Changes in
RL, Rti, and Raw were evaluated during vagal stimulation at increasing frequency before and after NO synthase blockade with N
-nitro-L-arginine methyl ester
(L-NAME). Vagal stimulation increased RL by
elevating both Rti and Raw. NO synthase blockade significantly increased baseline Rti, but not Raw, and significantly augmented the
effects of vagal stimulation on both Rti and Raw. Vagal stimulation also resulted in a significant increase in cGMP levels in lung tissue
before, but not after, L-NAME infusion. In seven additional piglets after RL was elevated by histamine infusion in the
presence of cholinergic blockade with atropine, vagal stimulation
failed to elicit any change in RL, Rti, or Raw. Therefore,
endogenous NO not only plays a role in modulating baseline Rti, but it
opposes the excitatory cholinergic effects on both the tissue and
airway components of RL. We speculate that activation of
the NO/cGMP pathway during cholinergic stimulation plays an important
role in modulating peripheral as well as central contractile elements in the developing lung.
lung resistance; development; maturation
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