Mechanisms of wood smoke-induced increases in nasal airway resistance and reactivity in rats.

We investigated the mechanisms of wood smoke-induced increases in nasal airway resistance (RNA) and airway reactivity in anesthetized rats. Delivery of wood smoke into a functionally isolated nasal airway produced an increase in RNA, which was attenuated by CP-96,345 [a tachykinin NK(1) receptor antagonist; (2S,3S)-cis-2-(diphenylmethyl)-N-((2-methoxyphenyl)-methyl)-1-azabicyclo(2.2.2.)-octan-3-amine] or atropine. Additionally, smoke pre-exposure animals displayed a greater amplitude and a longer duration of RNA responses to capsaicin or histamine provocation, as compared to air controls. This enhanced airway reactivity to capsaicin or histamine was largely alleviated by CP-96,345 or atropine. The nasal secretory responses to capsaicin or histamine in smoke pre-exposure animals were similar to those in air controls. We concluded that (1) reflex cholinergic and tachykininergic mechanisms play important roles in wood smoke-induced increases in nasal airway resistance and airway reactivity, and (2) this nasal airway hyperreactivity might not be due to an exaggerated secretory response, but is presumably due to augmented nasal swelling.