Conclusions
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1.
The increase of macromolecular leakage from the airway mucosa into the airway lumen can be significantly counteracted by locally applied BUD 4 μg/kg.
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2.
The same dose of 4 μg/kg, when administered via intravenous route or to distal trachea and bronchi, is without effect on BRAD-induced leakage.
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3.
(1)–(2) imply that tracheally applied BUD exerts its anti-permability effect, at such a low dose, strictly at application site and does not act by the part available to the systemic or pulmonary-bronchial circulation. Probably, it influences directly tracheal epithelial lining and affects endothelium of tracheal postcapillary venules.
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4.
The anti-permeability action is not reproduced by 10 min superfusion with progesterone 3×10−6 M, supporting a selective GCS mechanism by topical BUD.
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5.
Our results suggest that inhalation of selected GCS will lead to a rapidly triggered but protracted anti-inflammatory action on airway mucosa. After triggering, the GCS can be absorbed and inactivated through biotransformation (“hit and run” type of activity).
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6.
The presented rat tracheal model permits the continuous and precise (area, time) topical application of drugs to airway mucosa. Permeability studies can then be performed on the same airway segment.
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Miller-Larsson, A., Brattsand, R. Topical anti-inflammatory activity of the glucocorticoid budesonide on airway mucosa. Evidence for a “hit and run” type of activity. Agents and Actions 29, 127–129 (1990). https://doi.org/10.1007/BF01964740
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DOI: https://doi.org/10.1007/BF01964740