Changes in pulmonary lipoprotein lipase activity in dogs following experimental bone fracture. A new concept on the pathogenesis of post-traumatic impairment of lung surfactant synthesis and accumulation of fat in lung vessels?

Five hours after a limited, nonhypotensive trauma without gross interference with coagulopathy, lungs of dogs were found to be completely deficient of heparin-releasable, metabolically active lipoprotein lipase. This indicates that the pathway of circulating lipoprotein triglyceride hydrolysis as a source of palmitate for pulmonary dipalmitoyllecithin synthesis is blocked post-traumatically. The possible significance of this finding on post-traumatic impairment of pulmonary surfactant synthesis and accumulation of fatty material in the pulmonary capillary bed is discussed.