Dual effect of prostaglandin E2 on normal airways smooth muscle in vivo.

Inhalation of prostaglandin E2 by nonnal subjects caused initial bronchoconstriction followed by the predominant effect of bronchodilatation, which was maximal by 15 minutes. The degree of bronchoconstriction seen in the early phase appeared to be related to the initial tone of airways smooth muscle and was exaggerated after bronchodilatation with a large dose of ipratropium bromide. Bronchoconstriction induced by prostaglandin E2 is a direct effect on muscle and not secondary to a vagal reflex initiated by airways irritant receptors. Prostaglandin E2 (PGE2) is generally thought of as a bronchodilator agent. ' In vitro, however, it has been shown to have contractile as well as relaxant effects on airways smooth muscle.2 The balance between these antagonistic actions ofPGE2 may be influenced by the pre-existing tone of the muscle.3 In asthmatic patients a bronchoconstrictor action of inhaled PGE2 has also been described,4' which cannot be blocked by atropine.6 There is little information in published reports on the time course of the action of inhaled PGE2 in normal human airways. In patients with asthma a small dose of PGE2 caused variable initial bronchoconstriction five minutes after inhalation, bronchodilatation occurring subsequently and being maximal at about 15 minutes.7 The aim of this study was to analyse in detail the actions ofPGE2 on airways calibre in normal subjects and to determine the influence on this of airways smooth muscle tone.