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/l per s (mean ± SE). One day after ozone exposure (0.7-1,2 ppm; 2h), the base-line RL was not significantly changed (P>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<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/l per s before ozone, and this was not significantly different after ozone (4.5 ±1.1 cmH2O/l per s; P>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>0.5). Since both atropine and vagal cooling abolished the ozone-induced bronchial hyperirritability, we conclude that it is mediated via vagal cholinergic pathways.
|Number of pages||6|
|Journal||Journal of Applied Physiology Respiratory Environmental and Exercise Physiology|
|State||Published - 1977|
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