Increased nitric oxide biosynthesis in leukotoxin,9,10-epoxy-12-octadecenoate injured lung.

We measured effluent nitric oxide levels using a chemiluminescence method from leukotoxin (Lx, a linoleate epoxide) injured isolated rat lungs perfused with physiological salt solution. Nitric oxide production from Lx-injured lung promptly increased and lasted for 20 min. Pretreatment with NG-monomethyl-L-arginine (LNMMA) significantly suppressed Lx-induced production of nitric oxide. Effluent from control lungs showed trace levels of nitric oxide. The wet to dry lung weight (WLW/DLW) after termination of the experiments was significantly elevated in Lx-treated lungs compared with that of LNMMA pretreated lungs or control lungs. There was a correlation between nitric oxide levels (at 10 min) and lung edema (WLW/DLW). Thus, nitric oxide plays a role in the pathogenesis of Lx-induced lung injury.