Functional deficiency of pulmonary surfactant in the newborn infant

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In order to elucidate the pathophysiology of functional deficiency of pulmonary surfactant in the newborn infants, an animal model of acute respiratory distress syndrome was produced in the newborn piglet by the administration of endotoxin (lipopolysaccharides : LPS) via trachea. In this animal model, multiple organ failure was eliminated and solely the lung pathology similar to human ARDS due to septicemia could be achieved. The lung pathology was confirmed by the decreased surface activity, progressive hypoxemia and hypercarbia, decreased lung compliance, increased O_2 productivity, increased elastase activity, and increased lipid peroxides in bronchoalveolar lavage fluid (BAIF). Lung pathology was confirmed also by histological examination on autopsy.Then, the effect of prophylactically and therapeutically administered recombinant human superoxide dismutase (rh-SOD) on acute lung injury was evaluated. The prophylactic intratracheal administration of rh- SOD for lung injury caused by endotoxin was effective, It was confirmed by the maintenance of normoxemia and normocapnia, and lung compliance, and decreased production of lipid peroxides. Histologic examination also showed that the degrees of lung injury were milder in SOD pretreated animals.However, after the formation of lung injury, the intratracheal administration of rh-SOD was no more effective on the improvement.