Dibutyryl cAMP, aminophylline, and beta-adrenergic agonists protect against pulmonary edema caused by phosgene

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Abstract
Phosgene is a toxic oxidant gas that causes the adult respiratory distress syndrome in exposed workers. Phogene exposure markedly increased lung weight gain in buffer-perfused isolated rabbit lungs (31 .+-. 5 g over 60 min after phosgene vs. 7.7 .+-. 1.2 in control lungs, P < 0.01) and markedly increased the lung leak index for 125I-albumin (0.28 .+-. 0.03 after phosgene vs. 0.02 .+-. 0.01 in control lungs, P < 0.01). Pretreatment with dibutyryl adenosine 3'',5''-cyclic monophosphate (DBcAMP), aminophyline, or terbutaline plus isoproterenol prevented the increase in lung weight caused by phosgene (31 .+-. 5 g phosgene, 11.7 .+-. 2.8 DBcAMP, 7.5 .+-. 2.5 aminophylline, 6.1 .+-. 1 terbutaline and isoproterenol, 6.1 .+-. 1.2 control + aminophylline, and 7.7 .+-. 1.2 control; all treatments were P < 0.01 vs. the untreated phosgene group and not significantly different from control lungs). Pretreatment with aminophylline prevented the increase in lung leak index for 125I-albumin (0.28 .+-. 0.03 after phosgene vs. 0.06 .+-. 0.02 in aminophylline-treated lungs P < 0.01). Posttreatment with aminophylline and terbutaline also prevented the increase in lung weight caused by phosgene. These results indicate that phosgene dramatically increases the movement of fluid and protein across the pulmonary vasculature and that treatment with DBcAMP, aminophylline, terbutaline, or isoproterenol markedly reduces the pulmonary edema caused by phosgene.