Sensory-nerve-mediated nasal vasodilatory response to inspired acetaldehyde and acetic acid vapors

This study was designed to characterize the acute nasal vasodilatory respon ses to the sensory irritants acetaldehyde and acetic acid. For this purpose , the upper respiratory tract of the urethane-anesthetized male F344 rat wa s isolated by insertion of an endotracheal cannula, and irritant-laden air was drawn continuously through that site at a flow rate of 100 ml/min for 5 0 min. Vascular function was monitored by measuring inert vapor ( acetone) uptake throughout the exposure. Both acetaldehyde and acetic acid induced a n immediate concentration-dependent vasodilation as indicated by increased steady-state acetone uptake rates. This response was observed at exposure c oncentrations of 25 ppm or 130 ppm or higher for acetaldehyde or acetic aci d, respectively. The response to either vapor was significantly diminished in rats pretreated with the sensory nerve toxin capsaicin ( 50 mg/kg, 7 day s prior to exposure), providing evidence that sensory nerves play a role in the response. Acetaldehyde is metabolized by aldehyde dehydrogenase to ace tic acid. Pretreatment with the aldehyde dehydrogenase inhibitor cyanamide (10 mg/kg, 1 h prior to exposure) reduced the vasodilatory response to 200 ppm but not to 50 ppm acetaldehyde. These results suggest that formation of acetic acid is important in the sensory nerve-mediated vasodilatory respon se to high, but perhaps not to low, concentrations of acetaldehyde.