Sensory nerve-mediated immediate nasal responses to inspired acrolein

To investigate the role of sensory C-fiber stimulation and tachykinin relea se in the immediate nasal responses to the sensory irritant acrolein, the u pper respiratory tract of the urethan-anesthetized male Fischer 344 rat was isolated via insertion of an endotracheal tube, and acrolein-laden air [2, 5, 10, or 20 parts/million (ppm)] was drawn continuously through that site at a flow rate of 100 ml/min for 50 min. Uptake of the inert vapor acetone was measured throughout the exposure to assess nasal vascular function. Pl asma protein extravasation into nasal tissue and nasal lavage fluid was als o assessed via injection of Evans blue dye. At 20 ppm, acrolein induced 1) a twofold increase in acetone uptake, indicative of vasodilation, followed by a progressive decline toward basal levels and 2) increased plasma protei n extravasation, as indicated by dye leakage into nasal tissue and nasal la vage. These responses were inhibited by capsaicin pretreatment and the neur okinin type 1 antagonist N-acetyltrifluoromethyl tryptophan benzyl ester an d were potentiated by the peptidase inhibitors phosphoramidon and captopril , suggesting that these responses were mediated by tachykinin. At lower exp osure concentrations, acrolein was without effect on dye leakage but produc ed vasodilation, as indicated by increased acetone uptake. The responses at the lower concentrations were inhibited by capsaicin pretreatment, implica ting nasal sensory C-fiber involvement, but were not influenced by N-acetyl trifluoromethyl tryptophan benzyl ester, phosphoramidon, or captopril, sugg esting the involvement of a mediator other than the tachykinins substance P and neurokinin A.