Author/Authors :
Joad J. P.، نويسنده , , Mcdonald R. J.، نويسنده , , Giri S. N.، نويسنده , , Bric J. M.، نويسنده ,
Abstract :
In whole animals, ozone acutely impairs pulmonary function, an effect which may be mediated by eicosanoids. This study determined if the lung itself, separated from blood components and the CNS, responds to ozone with increased eicosanoid production and decreased function. Wistar rat lungs were placed in a negatively ventilated, buffer-perfused, isolated system, where they were exposed to filtered air or 1 ppm ozone for 3 hr. Ozone increased lung resistance (P = 0.02) and decreased dynamic compliance (P = 0.003, multivariate ANOVA for repeated measures). Pulmonary artery pressure, lung weight/body weight, and cells in lung lavage (BALF) did not change. In the perfusate, ozone increased the concentration of 6-keto-PGF(1α), PGF2α, PGD2, and TxB2 (all P < 0.05, t test) but not LTC4/D4 or PGE2. In BALF, ozone did not change the concentrations of any of the arachidonic acid metabolites tested (PGE2, 6-keto-PGF1α, PGD2, or LTC4/D4). We conclude that ozone increased intravascular concentrations of some cyclooxygenase products in the isolated buffer-perfused lung, an effect associated with reduced lung function.