RESUMEN
The purpose of this experiment is to evaluate the histopathologic findings of shark liver oil-induced lipoid pneumonia, and to determine whether shark liver oil is absorbed through lymphatics and the venous system or not. A single intratracheal administration of shark liver oil (0.6 ml/kg of B.W.) was given to Sprague-Dawley rats. They were then sacrificed sequentially from 1 hour to 12 weeks after injection. We investigated the chest radiographic findings, the serum total lipid concentration of blood obtained by cardiac puncture, lipid-laden alveolar macrophage index of the bronchoalveolar lavage fluid, and the histopathology of tracheobronchial lymph nodes and the lung (Oil red O stain & H&E stain). Chest radiographs showed no specific findings; ill-defined hazy, linear, small patch radioopacity, air space consolidation or collapse. Thirty-six percent of the experimental rats revealed normal findings. Within the lung, the shark liver oil appeared either as highly emulsified fine granules in the cytoplasm of the alveolar macrophage or as free, round oil masses. The area of the lung accumulated with lipid material was maximized 1 week after injection, and then decreased thereafter. The tissue reactions were cuboidal metaplasia of the alveolar lining, widening and lymphocytic infiltration of the alveolar septa and granuloma formation (3% of experimental rats) as a reaction to a foreign body. There were also lung abscesses due to superimposed bacterial infection (5% of experimental rats). With time after the injection of the oil, the serum total lipid tended to increase and the intracellular lipid of the alveolar macrophages in the bronchoalveolar lavage fluid tended to decrease. In summary, the histopathologic findings of the lung in the experimental lipoid pneumonia were interstitial chronic inflammation and granulomas with the presence of lipoid material in the lung parenchyma, and shark liver oil appeared to be absorbed in the blood and the lymph, then metabolized.