Differences between inhaled and intravenous bronchial challenge to detect O-3-induced hyperresponsiveness

Ozone (O-3)-induced airway hyperresponsiveness in laboratory animals is usu ally demonstrated through dose-response curves with inhaled or intravenous bronchoconstrictor agonists. However, comparability of these two routes has not been well documented. Thus guinea pig airway responsiveness to ACh and histamine was evaluated 16-18 h after O-3 (3 parts/million, 1 h) or air ex posure by two plethysmographic methods (spontaneously breathing and mechani cally ventilated) and by two administration routes (inhalatory or intraveno us). We found that O-3 caused airway hyperresponsiveness to intravenous, bu t not to inhaled, agonists, independent of the plethysmographic method used . Suitability of the inhalatory route to detect airway hyperresponsiveness was corroborated with inhaled ACh after an antigen challenge or extending O -3 exposure to 3 h. Acetylcholinesterase activity was not modified after O- 3 exposure in lung homogenates and blood samples. Thus inhaled agonists wer e less effective to reveal the airway hyperresponsiveness after an acute O- 3 exposure than intravenous ones, at least for the 1-h exposure to 3 parts/ million, and this difference seems not to be related to an O-3-induced inhi bition of the acetylcholinesterase activity.