The fine structures of vascular endothelial surface with linear endothelial folds, were clearly shown by scanning and transmission electron microscopes in large arteries and veins of man and other mammals and the nuclear parts of endothelial cells were shown in the gullies in scanning electron microscopical observation.
The effects of substances promoting or inhibiting transendothelial leakage were studied in relation to these structures. Immediately after the challenge their nuclear parts were transiently enlarged and prolonged and the linear endothelial folds became irregular by edematous swelling of endothelial cells and subendothelial structures. Pyridinolcarbamate pretreatment prevented these changes.
Administration of cholesterol for 2 weeks induced edematous and spherical change of endothelial cells of aorta; and then localized flat lesions of endothelial cells with flattening of their degenerated nuclear parts in localized areas exposed to mechanical stress from the arterial blood stream. After 3 to 4 weeks the flat lesions changed into elevated lesions, fatty spots or streaks. These endothelial changes were significantly inhibited by pyridinolcarbamate.
At the margin of the elevated lesions, nuclear parts of the endothelial cells were exposed on the endothelial fold by elevation of gullies. The exposed nuclear part exhibited a highly deformed and swollen shape and such changes may be followed by an increase in local transendothelial infiltration resulting in expansion of elevated lesions. Chemical inJuries induce weakness of the resistance of endothelial cells and the mechanical stress from the arterial blood stream may aggravate the injury in a special area facing the strong mechanical stress from the blood stream. Summation of such injuries may initiate atherosclerosis in such a special area followed by expansion of atherosclerotic lesion to all directions.