MECHANISM OF RAPID, SHALLOW BREATHING AFTER OZONE EXPOSURE IN CONSCIOUS DOGS

In 10 experiments on 3 conscious dogs exercising on a treadmill, we studied the effect of ozone on base-line ventilation and on ventilatory responses to inhaled bronchoconstrictor drugs. Prior to ozone exposure, inhalation of histamine diphosphate aerosol (1%; 5 breaths) increased respiratory frequency (f) by 86 ± % (mean ± SE), and inhalation of prostaglandin F(2α) (PGF(2α)) aerosol (0.1%; 5 breaths) increased f by 74 ± 16%. Immediately after ozone exposure (0.65 ppm; 2 h), steady-state base line f was increased by 120 ± 18% and tidal volume (V(T)) was decreased by 43 ± 5%. When conduction in the cervical vagus nerves (that were exteriorized permanently in skin loops) was blocked by cooling, these changes caused by ozone were abolished (P > 0.05). The increased responses to both histamine and PGF(2α) aerosols after ozone were unaffected by pretreatment of isoproterenol aerosol (0.5; 15 breaths), but were completely abolished by vagal cooling. Our studies indicate that ozone-induced rapid, shallow breathing and the increased ventilatory responses to inhaled histamine and PGF(2α) aerosols are mediated through vagal afferent pathways.