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 +/- 11% (mean +/- SE), and inhalation of prostaglandin F2 alpha (PGF2 alpha) 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 (VT) 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 greater than 0.05). The increased responses to both histamine and PGF2 alpha 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 PGF2 alpha aerosols are mediated through vagal afferent pathways.

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