In order to elucidate the mechanism of structural damage done to the arterial wall in arteriosclerosis or the mechanism of atheromatosis, we have concerned ourselves with histochemical determination of arterial wall constituents by microspectrophotometry. In the present study we investigated into the relationship between the tissue levels of elastin, collagen and glycoprotein in the media of the carotid artery and characteristics of sclerosis on the one hand and age on the other.
Common carotid artery specimens that were obtained in 83 controls aged 0 to 79 years and 33 patients with arteriosclerosis aged 50 to 79 were stained in several ways and assayed by microspectrophotometry.
The arterial media from controls was hardly hypertrophic but rich in elastin, soft and elastic, whereas for the sclerotic media the elastic fibers pursued a disorderly course and were fissured and levels of elastin in damaged tissue were markedly diminished. Histochemical study revealed that arterial tissue levels of elastin were progressively higher with increasing age in the age bracket of 0 to 20 years. After reaching a reak at age 20, arterial tissue levels of elastin showed a tendency to decline till age 30. After age 50 there were marked individual variations, and under a light microscope arterial tissue levels of elastin were remarkably diminished. Collagen in controls was found clinging to the media and adjacent to the smooth muscle, but in small quantities, while in sclerotic subjects confluently swollen collagen proliferation was noted. Histochemical assay indicated that arterial tissue levels of collagen rose in a steep curve, starting with age 0, and that a peak level was reached at age 20. After age 20 arterial tissue levels of collagen declined in a slow curve. After age 50 individual characteristics of sclerosis were more marked in sclerotic subjects than in controls, the former indicating a morbid increase in collagen.
Glycoprotein in controls was sparse and found uniformly distributed in the connective tissue and around voids in the smooth muscle, while in sclerotic subjects a great deal of confluent glycoprotein was present in layers in the middle or deeper intima. Histochemical assay in controls indicated that arterial tissue levels of glycoprotein were progressively increased between ages 0 and 10, but showed a nearly fixed tendency after age 20. In sclerotic subjects, on the other hand, arterial tissue levels of glycoprotein were significantly elevated after age 50.
For the group of controls the arterial tissue levels of elastin rose in a steep curve with increasing age till age 20 and declined in a slow curve thereafter. Collagen rose in a gentle curve till age 20 and declined also in a slow curve thereafter. Glycoprotein rose in a slow curve till age 20, and showed a fixed tendency thereafter. For the group of sclerotic subjects, on the other hand, the arterial wall constituents were found having a complicated diphasic change, with elastin being markedly diminished and other two constituents showing a morbid proliferation in conditions of tissue damage and being diminished in late course of the disease.
