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.