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ULTRASTRUCTURAL STUDIES ON HUMAN ARTERIOSCLEROSIS‐COMPARISON BETWEEN HYPERTENSIVE AND NORMOTENSIVE GROUPS
Author(s) -
Takebayashi Shigeo,
Kamio Akinori
Publication year - 1969
Publication title -
acta patholigica japonica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
ISSN - 0001-6632
DOI - 10.1111/j.1440-1827.1969.tb00091.x
Subject(s) - internal elastic lamina , arteriosclerosis , pathology , anatomy , atrophy , perfusion , medicine , adventitia , artery , myocyte , electron microscope , physics , optics
Systematic observation of arteriosclerosis by electron microscope was made on small arteries and arterioles of the stomach which were respected from 5 hypertensive cases and 6 normotensive cases who underwent surgery for gastric carcinoma or ulcer and which were fixed by perfusion with glutaraldehyde. Concurrently, three rabbits were used for animal experiments. Upon placing electrodes in the gastric wall of the rabbits, electric stimulation with 2.0 volt D.C. was repeated intermittently during the period of 5 to 12 days. Repeated contraction of vessels resulted in crush‐up effect of smooth muscle cells beneath the internal elastic lamina and in transition of irregularly minced cytoplasms into small osmophilic particles. At the same time dark cells appeared among the smooth muscle cells in the vicinity. The same findings were frequently noted in the lesions of gastric artery of man particularly in the hypertensive group. It was apparent that repeated angiospasm is an important factor for the histogenesis of sclerotic vascular lesion. The cells proliferating beneath the endothelial cells in arteriosclerosis were smooth muscle cells, and the direction of the proliferated smooth muscle cell layers did not necessarily conform with that of the media. They originated in the media and penetrated through the fenestrae of the internal elastic lamina. Fibrinoid necrosis and hyalinous thickening of arterioles were observed fairly frequently in the hypertensive group but always accompanied with intensive irregular atrophy or disappearance of the medial smooth muscle cells. Vascular lesions with initial thickening showed formation of new elastic lamina most of which was elastic fibers consisting of microfibrillar components. The additional formation of elastic fibers was particularly strong in the hypertensive group as the whole.

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