Am. J. Respir. Crit. Care Med., Vol 153, No. 2, Feb 1996, 604-609.
Inhaled nitric oxide attenuates bronchoconstriction in canine peripheral airways
DR Gwyn, KS Lindeman and CA Hirshman
Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland, USA.
Inhaled nitric oxide has been proposed as a bronchodilator because it
relaxes vascular and airway smooth muscle and attenuates cholinergic
reflexes. Although inhaled nitric oxide has been shown to act as a
bronchodilator in central airways, effects on peripheral airways are
largely unknown. To determine whether nitric oxide produces direct
relaxation of peripheral airways, we investigated the ability of nitric
oxide to attenuate hypocapnia- and acetylcholine-induced constriction in
the peripheral airways of anesthetized dogs. Peripheral airway resistance
(RP) was measured using a wedged bronchoscope technique. RP was increased
by either hypocapnia (0% CO2 through the bronchoscope for 3 min) or by
aerosolized acetylcholine (30 to 60 micrograms/ml for 1 to 3 min), in the
presence or absence of nitric oxide. Nitric oxide was delivered directly to
the lung periphery in the absence of O2. Nitric oxide (14.5 to 250 ppm)
attenuated responses to hypocapnia by 38 +/- 0 to 74 +/- 0% (n = 6) and to
acetylcholine by 36 +/- 0 to 52 +/- 0% (n = 6). The ability of inhaled
nitric oxide (< 100 ppm) to attenuate Rp responses to two different
direct-acting stimuli suggests that nitric oxide acts as a bronchodilator
in the lung periphery. The mechanism for this effect may involve relaxation
of airway and/or vascular smooth muscle.
