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Biomedical subjects

P T Andersson

Publications and source records attributed to P T Andersson.

2 recordsLinked to original sources

Budesonide reduces sensitivity to antigen but does not alter baseline tone or responsiveness to carbachol, terbutaline, and enprofylline in IgE-sensitized guinea-pig tracheae.

In vitro incubation of IgE-sensitized guinea-pig tracheal rings with 10(-7) M budesonide for 24 h significantly shifted the concentration-response curve to antigen by 5-fold to the right. Smooth muscle characteristics such as baseline tone, muscarinic contraction or relaxation to beta 2-receptor agonists and xanthines were not or only marginally affected by this exposure of airway tissue to a glucocorticoid drug. It is concluded that budesonide reduced anaphylactic IgE-driven release of contractile mediators.

Airway Resistance↗

Developments in anti-asthma glucocorticoids.

Studies carried out by Swedish and English workers in the mid 1950s appear to be the first successful uses of topical glucocorticoids in asthma. As shown with beclomethasone dipropionate during the 1970s, and expanded with budesonide during the 1980s, inhaled glucocorticoids have a very broad clinical efficacy and are safe to use. With increasing lung selectivity glucocorticoid drugs may well become a primary treatment for asthma. Even prolonged treatment with large doses of budesonide may not affect the contractile and relaxant characteristics of airway smooth muscle suggesting that this tissue is not a direct target for glucocorticoid actions. In IgE-sensitized guinea-pigs, as in atopic asthmatics, inhalational budesonide and other glucocorticoids inhibit both immediate and late phase pulmonary reactions occurring after allergen provocation. The anti-anaphylactic lung effects of glucocorticoids are not necessarily associated with inhibition of histamine and leukotriene release and, although PAF release was reduced by budesonide, the importance of this effect is as yet unknown. Airway eosinophilia is seen at the late phase reaction but may not consistently be reduced by glucocorticoids. These drugs reduce plasma leakage that is associated with both atopic and non-atopic asthma. Hence, a stabilising effect on airway endothelial-epithelial barriers may be one of the significant actions of glucocorticoids in the inflamed airways of patients with asthma or chronic obstructive pulmonary disease.

Administration, Inhalation↗