title: Effect of ozone on bronchomotor response to inhaled histamine aerosol in dogs.
abstract: 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.
mesh_terms: D000336:Aerosols; D000403:Airway Resistance / Q000187:drug effects*; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001980:Bronchi / Q000187:drug effects* / Q000294:innervation; D002799:Cholinergic Fibers / Q000502:physiology; D004285:Dogs; D006632:Histamine / Q000494:pharmacology*; D010126:Ozone / Q000494:pharmacology*; D014630:Vagus Nerve / Q000502:physiology*
chemical_list: D000336:Aerosols; D010126:Ozone; D001285:Atropine; D006632:Histamine