It is characteristic of arteries that they do not obey Hooke's law, but resist further stretch more strongly, the more they are stretched. It appears that this might be due to the combination of elastin fibers in the elastic laminae, with the much less distensible collagenous libers in the media and adventitia, more and more of which reach their 'unstretched length' as distension is increased. This has been verified on human iliac arteries, from autopsy, by comparing the 'elastic diagrams' (tension vs. circumference) before and after differential digestion of collagen by formic acid, and digestion of elastin by crude trypsin (containing an elastase). This proved that the resistance to stretch at low pressures was almost entirely due to elastin fibers, that at physiological pressures due to both collagenous and elastin fibers, but dominantly to collagen, and that at high pressures almost entirely due to collagenous fibers. In future work on the effect of age on the elasticity of iliac arteries, the initial slope of the elastic diagram can be taken as an index of the state, or number, of the elastin fibers, and the final slope as an index of the state, or number, of collagenous fibers.

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It is characteristic of arteries that they do not obey Hooke's law, but resist further stretch more strongly, the more they are stretched. It appears that this might be due to the combination of elastin fibers in the elastic laminae, with the much less distensible collagenous libers in the media and adventitia, more and more of which reach their 'unstretched length' as distension is increased. This has been verified on human iliac arteries, from autopsy, by comparing the 'elastic diagrams' (tension vs. circumference) before and after differential digestion of collagen by formic acid, and digestion of elastin by crude trypsin (containing an elastase). This proved that the resistance to stretch at low pressures was almost entirely due to elastin fibers, that at physiological pressures due to both collagenous and elastin fibers, but dominantly to collagen, and that at high pressures almost entirely due to collagenous fibers. In future work on the effect of age on the elasticity of iliac arteries, the initial slope of the elastic diagram can be taken as an index of the state, or number, of the elastin fibers, and the final slope as an index of the state, or number, of collagenous fibers.

Static pressure–volume curves were done on seven intracranial saccular aneurysms and 16 major cerebral arteries from human autopsies. The aneurysms were much less distensible than the arteries. The major change was in the initial or elastin part of the curve (elastance of 6 ± 5 S.D. × 105 dynes/cm per 100% elongation in the artery compared to 13.5 ± 5 × 105 dynes/cm per 100% elongation for the aneurysm; p < 0.005). This agrees well with histological studies which show that elastin is decreased and fragmented in aneurysms.As the aneurysm enlarges, its wall must become thinner. This change, coupled with the loss of distensibility, makes it more prone to rupture. Obviously the larger the aneurysm, the thinner the wall (if the volume of tissue remains constant), and the greater the risk of rupture.The distensibility of major cerebral arteries could be dramatically decreased by two or three runs to pressures of 200 mm Hg. The elastance of the initial part of the curve changed from 2 ± 1 × 105 dynes/cm per 100%; elongation to 8 ± 1 × 105 dynes/cm per 100% elongation (different at p < 0.001). The final elastance was altered less significantly (42 ± 6 × 105 dynes/cm per 100% elongation to 82 ± 28 × 105 dynes/cm per 100% elongation; p < 0.01). This shift in distensibility was accompanied by a significant increase in diameter of the artery. High pressures appear able to break the single elastin layer of cerebral arteries.

The Hemodynamic Importance of the Geometry of Bifurcations in the Circle of Willis (Glass Model Studies) • The critical Reynolds number, Re c , at which turbulence developed in glass model bifurcations was measured with an Evans blue indicator for bifurcations with a branch/trunk area ratio of unity, and bifurcation angles of 45°, 90°, 135°, and 180°. The Re c dropped from 2,500 in a straight tube to 1,200 in the 180° bifurcation. Further drops occurred with pulsatile flow (if the mean flow rate was used to calculate the velocity). Three sizes of aneurysms at the apex of the 90° bifurcation lowered the Re c to between 400 and 500 with a slight difference between steady and pulsatile flow. Reverse flow through the same bifurcation produced a more radical drop in the Re c at small bifurcations, and less in the 180° ones. The curves for steady and pulsatile flow crossed at 135°. We did qualitative, but not quantitative, assessments of axial stream impingement on the apex of the bifurcation in the site of aneurysm formation, and of boundary layer separation and vortex shedding at the lateral angles. Both appeared to vary with the angle of the bifurcation and the Reynolds number. We also studied flow profiles in glass models of anterior cerebral-anterior communicating artery bifurcations and the posterior communicating artery origin from the internal carotid. The relevance of these studies to localization of intimal cushions, aneurysms, and atherosclerosis was discussed.Additional Key Words atherosclerosis aneurysms turbulence vortex shedding boundary separation layer Reynolds number intimal cushions