An electron microscopic study of the fine blood vessels in the skin and muscle of 25 newborn rats (sucklings, and therefore subject to physiologic lipemia) has shown that blood-borne lipid particles may leave the lumen of these vessels by two pathways, intercellular and intracellular. (a) An intercellular pathway: Some capillaries, venous capillaries and venules contain intramural, extracellular deposits of lipid which is presumably hematogenous. In some animals these deposits are quite numerous; available evidence suggests that they are a consequence of intercellular gaps, too small or too transient to be observed except in rare instances. Plasma apparently escapes through these gaps and filters across the basement membrane, while lipid particles are retained, usually in sufficient number to fill the small defect; some lipid particles are then taken up by endothelial cells and pericytes, while a few escape and are incorporated into free phagocytes. These focal defects, though few in number, may explain the apparent incapacity of blood vessels of newborn rats to leak any further after a local injection of histamine. Discontinuities in the endothelium were found also in the renal glomerulus, sometimes accompanied by extensive interstitial accumulations of lipid particles. Similar intercellular gaps are known to exist in other types of immature endothelia. (b) An intracellular pathway: This is best demonstrated in the capillaries, venous capillaries and venules which supply the developing subcutaneous adipose tissue. Here the lipid particles adhere in large numbers to the endothelial surface; the morphologic evidence suggests that they are also taken up into the endothelium through phagocytosis by "flaps," or into pockets or crevices. The lipid is apparently metabolized in the vascular wall; some is found in the multivesicular bodies. There was no evidence of active transport by vesicles or vacuoles. Neither pathway was demonstrable in the adult.

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