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.
D000818:Animals; D001794:Blood Pressure; D004285:Dogs; D050723:Fractures, Bone; D006493:Heparin; D006614:Hindlimb / Q000293:injuries*; D008071:Lipoprotein Lipase / Q000378:metabolism*; D008168:Lung / Q000201:enzymology* / Q000473:pathology; D008297:Male; D011651:Pulmonary Artery; D011663:Pulmonary Surfactants / Q000096:biosynthesis*
D011663:Pulmonary Surfactants; D006493:Heparin; D008071:Lipoprotein Lipase