Fenestrations in the internal elastic lamina at bifurcations of human cerebral arteries.

Abstract

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 ...

The role of shear stress in the pathogenesis of atherosclerosis

“…Although the internal elastic lamina separates medial vascular SMC from the abluminal endothelium, numerous membrane pores (2-7 mm) permit direct communication between the endothelial cells and vascular SMC, potentially through myoepithelial bridges. 13,14 Interactions between these cell types are important for proper vessel wall function and both have been shown to be responsive to shear stress. For example, laminar shear stress inhibits not only endothelial but also vascular SMC proliferation.…”

Disturbed Laminar Blood Flow Vastly Augments Lipoprotein Retention in the Artery Wall

“…Further experiments are needed to clarify the upstream mechanisms relaying the mechanical force of blood into changes in lipoprotein binding of the arterial wall, as well as the relative importance of shear stress versus stretch in this process. Lowered wall shear stress has profound effects on endothelial cell phenotype, and it is conceivable that these may in turn influence local VSMCs to modulate and secrete lipoprotein-binding matrix through either direct contact 45,46 or paracrine mediators. 5,47 However, it is also possible that increased circumferential cyclic stretching of the artery wall, which is induced proximal to the constrictive collar and found at natural atherosclerosis-susceptible sites, 2 directly affects phenotypic characteristics of VSMCs.…”

Aneurysmal Remodeling in the Circle of Willis after Carotid Occlusion in an Experimental Model

“…The presentation of a rough and irregular endothelial surface has conventionally been interpreted as a sign of EC dysfunction. [26][27][28] Internal elastic lamina (IEL) fenestrations-raised circular lesions on the cast surface with defined boarders, representing indentations in the vessel lumen due to focal weakening of the IEL 29 or luminal matrix degradation. 21 Smooth muscle cell (SMC) imprints-striations perpendicular to the direction of flow that are indicative of massive IEL loss, which places the endothelial layer directly onto the medial layer such that imprints of the SMC structures are visible on the cast surface.…”