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Metabolism and Ultrastructure of the Arterial Wall in Atherosclerosis

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Abstract

SPONTANEOUS atherosclerosis in man begins as a disease of the arterial intima. The morphologic and functional individuality of this intimal lining and the peculiarities of its metabolic requirements and cytologic components have been recently confirmed by findings on biochemical examination and electron microscopic studies.1, 2

Although the large arteries of a four-month-old human embryo show three layers, intima, media, and adventitia, their structural evolution occurs gradually and the intima of the aorta is not fully differentiated until the end of the second decade. Indeed its final development may be contemporary with early regressive changes usually considered as senescent alterations, particularly deposition of collagen and subendothelial thickening. These changes may be at first symmetric, but are later made more pronounced by incorporation of elastic elements. They will eventually modify the geometry of the vascular lumen and introduce significant variations in local laminar blood flow.3,4

It is therefore difficult to describe the characteristics of the normal intimal lining of large arteries of adult human beings without mentioning some of its earliest pathologic changes.

One of the functionally significant properties of the normal vascular intima is its lack of capillary vessels. Adventitial vasa vasorum do not penetrate farther than the middle portion of the tunica media. This means that both the intima, from 100 to 130 μ thick in the adult human aorta, and the inner portion of the media depend for their nutrition on metabolites filtered from the arterial lumen. Recent in vitro studies on the transport of sodium and chloride in . . .


 

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