The experiments on dogs show that the bronchoconstriction after acetylcholine inhalation is caused by a reflex mechanism mediated via sensory receptors and N. vagi. Blockade of the N. vagi with low concentration of Novocain does not affect tidal volume and frequency but blocks the acetylcholine-induced bronchoconstriction. Higher concentration of Novocain, like vagotomy, also decreases the breathing frequency and increases the tidal volume.The arterial blood gases following acetylcholine inhalation are probably more influenced by the changes on the peripheral airways than by the influence on the more central airways which are more important for the airway resistance