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

SUMMARY Measurements of fenestrations (or windows) in tbeInternal elastic lamina at the bifurcation of human cerebral arteries, were obtained from photomicrographs (scanning electron miscroscope). Thirteen of 28 bifurcations rerealed regions of enlarged fenestrations among tbe normal fenestrations in tbe ridnity of the apex. Tbe mean diameter of the enlarged fenestradons (7.0 ± 034 SEM /an) was significantly greater dun die mean diameter (2.1 ± 0.13 SEM ftm) of die normal fenestrations. The number of fenestrations per sq mm was. less (2606 ± 284 SEM per sq mm) for the enlarged fenestrations than for tbe normal fenestrations (4518 ± 397 SEM per sq mm). The proportion of tbe area of internal elastic lamina comprised of fenestrations increased to 15.0 ± 1.1 SEM percent for tbe enlarged fenestradons from a mean of 1.8 ± 0.16 SEM percent for die normal fenestrations. Fenestradons from bifurcations without enlarged fenestrations, demonstrated characteristics similar to tbe normal fenestrations. More than 80% of tile specimens exhibited a gap in die internal elastic lamina in the apical region of die bifurcation. Based on a comparison of stress concentration factors, we propose that the presence of enlarged fenestrations represents a weakness in die internal elastic lamina at die bifurcation apex which may contribute to die initiation of mkroaneurysms.Stroke, Vol 12, No 4, 1981THE STRUCTURE of the internal elastic lamina of cerebral arteries has never been clearly delineated. In addition, the role of the internal elastic lamina in the formation of intracranial saccular aneurysms, known to form predominantly at bifurcations, remains an enigma. Dees 1 first described the internal clastic lamina of human and bovine aortas and renal arteries as a continuous sheath penetrated by small windows. However, Nystrom 1 described the elastic lamina of human arteries as a fibrous structure. Lang and Kidd' stated that the elastic lamina of human cerebral arteries is split into layers with the luminal surface a meshwork of fibers which transforms into a spongelike layer, and finally forms a solid mass in the layer adjacent to the media.Hassler 4 examined the fencstrations, which he described as windows, contained within the elastic lamina of cerebral arteries of humans, from newborns to the age of 90. He presented data to describe relevant characteristics of fenestrations in the internal elastic lamina of straight cylindrical segments isolated from the intracranial portion of the internal carotid and anterior cerebral arteries. Cook, Salmo, and Yates 8 examined the "length" and "number of gaps" in the internal elastic lamina of the external iliac artery from humans aged 20 to 70 years. Other authors'-•• T have made reference to fenestrations, but did not provide data concerning their characteristics. A subsequent paper by Hassler' showed large fenestrations at the neck of a saccular aneurysm obtained at autopsy. Nevertheless, specific information on the size of these fenestrations was not presented.The present study was undertaken in ...

Although the aorta normally functions under radial compressive stresses associated with lumen blood pressure, these results show that the aorta tears radially at a much lower value of stress than would have been predicted from previous studies that have reported longitudinal and circumferential Young's modulus. This could explain why dissections propagate readily once the initial tear occurs.

SUMMARY1. Hind limb blood flow was measured in lambs of from 91 days gestation (delivered by Caesarean section) to 1 month after birth (term is about 147 days), under chloralose anaesthesia. Vascular resistance/100 g wet wt. increased progressively with age. There was reflex femoral vascular tone from the earliest age studied, as shown by vasodilatation on cutting the sciatic nerve.2. On asphyxia by cord occlusion reflex femoral vasoconstriction began earlier and was somewhat greater in older foetal lambs. At all ages, and after denervation of the hind limb, there was vasodilatation after local ischaemia, and a vasoconstriction of delayed onset during asphyxia attributed to release of noradrenaline into the circulation. The vasoconstrictor effect of noradrenaline in immature lambs was at least as great as at term or in the new-born.3. Injections of minimal effective doses of cyanide were used to localize possible chemoreceptor sites in foetal lambs. Injection into the left atrium caused a rise of arterial pressure, femoral vasoconstriction and a complex change in heart rate (usually bradycardia) but rarely any respiratory movement. After atropine, cyanide caused a large tachycardia. All responses were much reduced or abolished by cervical vagotomy.4. Injection of the same doses of cyanide into a jugular vein, the right ventricle, pulmonary or common carotid arteries of foetal lambs caused