Lipid peroxidation and lung ultrastructural changes in an experimental model of leukocyte-mediated pulmonary injury
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The aim of this study was to study ultrastructural changes and lipid peroxidation in rabbits lung after massive complement activation and leukocyte aggregation. A prolonged and massive leukocyte activation was induced by intraperitoneal inoculation of zymosan suspended in paraffin. Fifteen animals (group 3) were given 0.6 g/kg of zymosan, 22 animals (group 2) received 1 g/kg, and 11 rabbits (group 1) were treated with paraffin alone and served as controls. An acute mortality rate of 40% was observed in group 3 and of 68% in group 2. Surviving animals were studied for 10 days. In these animals a marked decrease in circulating granulocytes and a progressive decline in arterial PO2 were recorded (PO2 on day 10 in group 2 animals was 51.94±4.26,p<0.01). Microscopic and ultrastructural evaluation revealed sequestration of granulocytes in the pulmonary microvasculature. Studies of lung homogenates demonstrated increased levels of lipid peroxide derivative malondialdehyde (group 2 rabbits, 1624±638; group 1, 795±57 pm/mg pt,p<.001) and decreased levels of the tissue antioxidant alpha-tocopherol. The results of this study are compatible with the hypothesis of leukocyte-mediated injury through production of oxygen radicals.
Key wordsLeukocytes Lipid peroxidation Pulmonary injury
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