An electron microscopic study of intestine and liver in rats ingesting a high-lipid diet or receiving corn oil by stomach tube was carried out. Studies of the intestinal phase of lipid absorption in rats showed what appears to be the direct transfer of particles across the cell membrane confirming the postulate that some of the process of lipid absorption involves triglyceride particles. Lipid droplets, representing chylomicrons were identified in hepatic sinusoids. They were traced into the pericellular space of Disse, which they had entered through the wide pore spaces in the sinusoidal endothelial cytoplasm. Lipid particles were also observed in different stages of direct transfer across the hepatic parenchymal cell membrane, and their formation of larger cytoplasmic lipid droplets within the cytoplasm of liver cells. This mechanism is proposed as a major device of the body in dispersing the lipemia which occurs after the ingestion of a fat meal.
The cutaneous lesions of adult rats with homologous disease are described, and evidence is presented to indicate that they have an immunologic basis. The skin changes included erythema, purpura, edema, and a variety of inflammatory lesions. In the more active lesions, dermal infiltration, hydropic degeneration, acanthosis, and atrophy of the epidermis with hyperkeratosis and follicular plugging were present. In some cases, ulceration and sloughing were also observed. More chronic lesions were characterized by atrophy of the epidermis and collagenization of the dermis with disappearance of the skin appendages.
Rejection of autografts was observed simultaneously with acceptance of homografts. The histologic appearance of autografts undergoing rejection was similar to that of the spontaneous skin lesions, suggesting that the latter, too, had an immunologic basis. In favor of this, also, was the specificity of the dermatitis for the skin of the host, with sparing of neighboring homograft tissue.
There was a histologic similarity between the spontaneous skin lesions of homologous disease and those of lupus erythematosus on the one hand, and scleroderma on the other, thus supporting the possibility that the cutaneous lesions of these connective tissue diseases of man may also have an immunologic basis.
It was concluded that the adult rat with homologous disease may furnish a model for human autoimmune disease.
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