Abstract
The effects of rabbit exposure to ozone (O3) (0.4 ppm for 4 h) on pulmonary mechanical properties and hemodynamics have been investigated on the isolated perfused lung model. Tracheal pressure, airflow, and tidal volume were measured in order to calculate lung resistance (RL) and dynamic compliance (Cdyn). Using the arterial/venous/double occlusion method, the total pressure gradient (ΔPt) was partitioned into four components (arterial, pre-, postcapillary and venous). Dose–response curves to acetylcholine (ACh), substance P (SP), and histamine were constructed in lungs isolated from rabbits immediately or 48 h after air or O3exposure. O3induced a significant increase in the baseline value of ΔPt, more markedly 48 h after the exposure. Immediately after the exposure, O3partly inhibited the ACh-, SP-, and histamine-induced decreases in Cdyn and increases in RL. This inhibitory effect was still in part present 48 h after O3treatment. In the groups studied immediately after exposure, O3did not significantly modify the ACh-, SP-, and histamine-induced vasoconstriction. Forty-eight hours after exposure, O3induced a contractile response to ACh and SP in the arterial segment but decreased the response to histamine. We conclude that O3can induce direct vascular constriction. Directly, but also 48 h after exposure, O3can inhibit the ACh-, SP-, and histamine-induced changes in lung mechanical properties. Ozone can also induce some changes in the intensity and in the location of the vascular responses to ACh, SP, and histamine.
Published Version
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