Chylomicron metabolism by normal and injured isolated rat lungs

Since the lung is the first highly vascularized organ to which chylomicrons are exposed, we sought to determine whether the lung vasculature is capable of metabolizing triglyceride contained in circulating, native chylomicrons. In addition, since acute lung injury can depress other endothelial cell associated metabolic functions, we determined whether acute injury due to alpha-naphthylthiourea (ANTU) changed chylomicron triglyceride metabolism by lungs. We compared the hydrolysis of radiolabelled chylomicrons from rat mesenteric lymph by perfused lungs isolated from rats pretreated with ANTU; with the vehicle, Tween 80, alone; or untreated control rats. In all groups of lungs, we found that perfusate content and concentration of triglyceride decreased over 30 minutes of perfusion, while that of free fatty acid increased, indicating that isolated lungs are able to hydrolyze chylomicron triglyceride. Despite enhancement of hydrolysis by perfusates containing 6 gm/100 ml of bovine serum albumin, there were no differences among the groups of lungs in the extent or rate of triglyceride metabolism. The [1-14C]-oleate from chylomicron triglyceride was taken up into lung tissue during 30 minutes of perfusion and incorporated into neutral lipid, phosphatidylcholine, and phosphatidylethanolamine to a similar degree by ANTU-injured and control lungs. Lipoprotein lipase activity in homogenates of lungs from ANTU and Tween treated rats did not differ. We conclude that lungs are capable of hydrolysis of triglyceride contained in chylomicrons and that this endothelial cell associated metabolic function is not altered by acute lung injury caused by ANTU.