Effect of ozone on bronchomotor response to inhaled histamine aerosol in dogs.

To study the effect of ozone on bronchial reactivity to inhaled histamine diphosphate aerosol, we performed 14 experiments on 5 dogs anesthetized with pentobarbital sodium (25-30 mg/kg, iv) and ventilated with a Harvard respirator. Prior to ozone exposure, inhalation of histamine aerosol (2% solution; 5 breaths) increased total pulmonary resistance (RL) 5.1 +/- 0.5 cmH2O/1 per s (mean +/- SE). One day after ozone exposure (0.7-1.2 ppm; 2 h), the base-line RL was not significantly changed (P greater than 0.05), but the increase of RL caused by histamine (10.7 +/- 1.1 cmH2O/1 per s) was greater than in the control state (P less than 0.01). When the dogs were pretreated with atropine sulfate aerosol (1.5% solution; 10 breaths), the increase of RL after histamine was decreased to 3.8 +/- 0.3 cmH2O/1 per s before ozone, and this was not significantly different after ozone (4.5 +/- 1.1 cmH2O/1 per s; P greater than 0.5). Cooling blockade of conduction in the vagus nerves diminished the increase of RL after histamine to 3.9 +/- 0.5 cmH2O/1 per s before ozone, and this was not significantly different after ozone (4.4 +/- 0.6 cmH2O/1 per s; P less than 0.5). Since both atropine and vagal cooling abolished the ozone-induced bronchial hyperirritability, we conclude that it is mediated via vagal cholinergic pathways.