Key result
Ligature of the common carotid artery caused intimal thickening principally due to the growth of smooth muscle-derived 'myo-intimal' cells, rather than endothelial hyperplasia.
Why the study?
The cellular origin and characteristics of intimal thickening after arterial ligature were not fully understood.
Answers are grounded in this paper and cite their sources.
This study identifies 'myo-intimal' cells derived from smooth muscle as the primary driver of intimal thickening following arterial ligation.
Concentric thickening of the tunica intima was observed in a short length of common carotid artery which had been tied off between two ligatures, and also in the pieces immediately proximal and distal to the doubly ligated part. The thickening was not due to hyperplasia of endothelial cells; in fact, the endothelium in the doubly ligated part was necrotic a short time after ligature. This piece then became lined with macrophage-like cells, thought to be derived from monocytes of the blood contained in the lumen. These cells retained quantities of colloidal thorium dioxide which had been given intravenously just be fore applying the ligatures. On the other hand, the thickening of the intima seen in the doubly ligated segment, as well as in the adjoining lengths of artery, was principally due to the growth of a cell derived from the smooth muscle of the tunica media, for which the term "myo-intimal" cell is suggested.
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Robert C. Buck (1961) studied Intimal thickening. Ligature of arteries was evaluated on Intimal thickening and cellular composition. Ligature of the common carotid artery caused intimal thickening principally due to the growth of smooth muscle-derived 'myo-intimal' cells, rather than endothelial hyperplasia.
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