An Analysis of Mechanisms of Post Stenotic Dilatation

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Abstract
In 107 chicks, circumferential ligatures were used to narrow the thoracic area to about 2/3 of its original caliber. The aortas of 101 unoperated chicks were used as controls. Within 2 weeks after surgery, macroscopic post stenotic dilatation was observed in some of the surgically treated aortas. The incidence increased with time. Proximal to the stenosis, the aortic wall showed increased thickness; distally, the wall was thinner than in the controls. At the region of most marked narrowing, intimal proliferation was marked with the formation of plaques, cushions, and valve-like fibrous structures. In the operated chicks which were fed a diet supplemented with cholesterol and oil, the accumulation of lipid in the aortic intima was more marked on the proximal side of the stenosis than on the distal side. In the stenotic ring, lipid was absent from the wall. These degrees of lipid infiltration correlated with the probable intravascular pressures in the 3 segments. These and related data support the thesis that post stenotic dilatation was not due to increased pressure. The enlargement of the lumen of blood vessels, as in post stenotic dilatations and aneurysms, and perhaps the normal growth of vessels, may be a result of increases in the drag force at the boundary layer of the blood stream which acts on the endothelium. The endothelial cells, while fixed to the intima, were considered to be sensitive to the drag forces. Model experiments consonant with the drag hypothesis were presented.