Intalipid® was administered intravenously to mice at a level of 2 g kg−1 day−1 for 23 days. No alterations in phagocytic index, liver or spleen size were observed in the chronically injected mice as compared with control mice that received saline injections. Tissue distribution of 0.45 μm multilamellar liposomes of egg phosphatidylcholine:cholesterol (2:1) was similar in mice that had been chronically injected with Intralipid® to that in control mice. Mice chronically given the same total amount of phospholipid in the form of 0.2 μm liposomes of phosphatidylcholine:cholesterol (2:1) rather than as a lipid-triglyceride emulsion showed altered tissue distribution of entrapped label with decreased liver uptake and increased splenic uptake, which is indicative of reticuloendothelial blockade. Tissue distribution of [14C]dipalmitoylphosphatidylcholine Intralipid® was compared with that of [14C]dipalmitoylphosphatidylcholine 0.2 μm MLV of phosphatidylcholine:cholesterol (2:1). Intralipid® was taken up 2- to 3-fold less by liver and 5- to 10-fold less by spleen than liposomes. Blood levels of Intralipid® were higher than those of liposomes. [14C]dipalmitoylphosphatidylcholine Intralipid® was eliminated from the body at a faster rate than [14C]dipalmitoylphosphatidylcholine liposomes. The lack of reticuloendothelial blockade caused by Intralipid® as compared with liposomes appears to be related to its diminished uptake into reticuloendothelial tissues. This diminished uptake may be related to differences in apolipoprotein uptake of Intralipid®, which is primarily in the form of a phospholipid monolayer, and liposomes, which have their phospholipid organized into a bilayer.
