| pubmed-article:8393949 | pubmed:abstractText | To elucidate the role of endogeneous cyclic AMP in the protection against airway mucosal dysfunction induced by air pollutants, we studied the effect of sulfur dioxide (SO2) on ciliary motility in rabbit cultured tracheal epithelium in vitro. Exposure of cells to perfusate bubbled with SO2 rapidly decreased ciliary beat frequency (CBF), as assessed by a photoelectric method, from 971 +/- 12 to 718 +/- 28 beats/min by 3 ppm SO2 and from 963 +/- 22 to 635 +/- 34 beats/min by 10 ppm SO2 (p < 0.001, in each case). This effect was reversed by washing out the SO2-containing medium and was accompanied by a corresponding decrease in intracellular levels of cyclic AMP. Preincubation of the epithelial cells with salbutamol, vasoactive intestinal peptide, prostaglandin E2 or 3-isobutyl-1-methylxanthine increased cyclic AMP levels and inhibited the decreases in both CBF and cyclic AMP in response to the subsequent application of SO2 at 3 ppm, whereas dexamethasone had no effect. These results suggest that SO2 decreases airway ciliary motility through the reduction of intracellular cyclic AMP concentration, and that drugs that increase endogeneous cyclic AMP may prevent the SO2-induced impairment of mucociliary transport in the respiratory tract. | lld:pubmed |
