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Abstract Acute lung injury in the rat has been produced by the deposition of immune complexes, by using the model developed earlier in this laboratory. The airway instillation of antibody (rabbit IgG) to bovine serum albumin (BSA) and the i.v. injection of BSA results in acute alveolar injury. As measured quantitatively by the leakage of 125l-rat IgG into the lung parenchyma, acute injury occurring over a 4-hr period can be markedly suppressed, in a dose-dependent manner, by the simultaneous airway instillation of antibody and catalase but not by chemically inactivated catalase, by superoxide dismutase (SOD), or by antiproteases (soybean trypsin inhibitor, a 1-antitrypsin inhibitor from human serum) that are known to be potent inhibitors of the neutral proteases derived from rat lysosomal granules. Instillation of radiolabeled catalase, SOD, α1-antitrypsin, and soybean trypsin inhibitor into lungs of normal rats reveal average lung retention rates at 3 hr of 67, 54, 84, and 83%, respectively, suggesting that the inability of antiproteases to protect from acute injury is not related to their rapid disappearance from the lung. By immunofluorescence, the catalase-suppressed lung reactions contain deposits of immune complexes. Histologically, the suppressed lung reactions contain infiltrates of neutrophils in an interstitial and intraalveolar location, but hemorrhage and intra-alveolar edema are absent. These studies suggest that a major mechanism for damage occurring in immune complex-triggered, complement and neutrophil-dependent acute lung injury may be related to the production of H202 and/or its metabolic products.
Johnson et al. (Mon,) studied this question.