Joad J P, McDonald R J, Giri S N, Bric J M
Department of Pediatrics, University of California at Davis 95616.
Environ Res. 1994 Aug;66(2):186-97. doi: 10.1006/enrs.1994.1054.
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-PGF1 alpha, PGF2 alpha, 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-PGF1 alpha, 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.
在完整动物中，臭氧会急性损害肺功能，这种效应可能由类花生酸介导。本研究确定了与血液成分和中枢神经系统分离的肺本身是否会对臭氧产生反应，表现为类花生酸生成增加和功能下降。将Wistar大鼠的肺置于负压通气、缓冲灌注的离体系统中，使其暴露于过滤空气或1 ppm臭氧中3小时。臭氧增加了肺阻力（P = 0.02）并降低了动态顺应性（P = 0.003，重复测量的多变量方差分析）。肺动脉压、肺重量/体重和肺灌洗（BALF）中的细胞数量没有变化。在灌注液中，臭氧增加了6-酮-PGF1α、PGF2α、PGD2和TXB2的浓度（所有P < 0.05，t检验），但没有增加LTC4/D4或PGE2的浓度。在BALF中，臭氧没有改变所测试的任何花生四烯酸代谢产物（PGE2、6-酮-PGF1α、PGD2或LTC4/D4）的浓度。我们得出结论，臭氧增加了离体缓冲灌注肺中一些环氧化酶产物的血管内浓度，这种效应与肺功能降低有关。
