Structural and Architectural Changes during Arterial Development and the Role of Hemodynamics

Abstract

Hemodynamics is a major determinant in the anatomical and mural architectural development of the arterial tree. Arterial intimal proliferation commences in utero at specific anatomical sites often appearing eccentric in transverse section and precedes more diffuse concentric thickening. Regarded as an inherent structural component of the wall or an adaptive mural response to increasing hemodynamic stresses concomitant with growth, its occurrence in utero and in lower animals, though generally supportive of this view, ignores qualitative changes. Further doubt derives from the retrogressive destructive nature of structural changes in the arterial wall in the young, individual differences and their continued progression after birth and maturation. It is postulated that concomitantly with arterial development the associated degenerative changes are attributable to hemodynamically induced bioengineering fatigue caused by longitudinal stretching and circumferential distensile effects of the pulse waves and by lesser vibrations generated by flow at sites of predilection for compensatory intimal thickening. This intimal proliferation is the compensatory reparative response to loss of tensile strength of mural constituents and of the vessel wall as a whole.

Enrichment of Genes in the Aortic Intima That Are Associated With Stratified Epithelium

“…The tunica intima is composed of a single layer of endothelium that lines the lumen, smooth muscle cells, and connective tissue; the major cell type of the intima is the intimal smooth muscle cell. 1 A surprising number of these arterial intima-enriched genes are also enriched in stratified epithelia, such as the epidermis. 17 A number of these represented precursors of the CE and proteins involved in adhesive junctions.…”

“…1,2 The vena cava and other veins have comparatively thin intima and media and sustain dramatically less pressure. 1 In fact, the predominant vascular feature when a vein is exposed to arterial flow is smooth muscle cell proliferation and matrix deposition that results in intimal thickening.…”

“…1,2 The vena cava and other veins have comparatively thin intima and media and sustain dramatically less pressure. 1 In fact, the predominant vascular feature when a vein is exposed to arterial flow is smooth muscle cell proliferation and matrix deposition that results in intimal thickening. 3,4 It is widely believed that at least some aspects of the differences in the functional phenotype of vascular components, including the vascular endothelium and intimal smooth muscle cells in arteries and veins, are related to these hemodynamic considerations.…”

“…For example, the earliest atherosclerotic lesions are limited to large elastic and muscular arteries. 1,7,8 Consequently, one of the major initiatives of vascular biology is to understand this functional and anatomic heterogeneity at a molecular level. 7,8 Because so little is known about the molecular differences between arteries and veins, we used high-density oligonucleotide arrays to analyze the transcriptional profile of the mouse aorta and inferior vena cava (IVC) to identify genes whose expression was enriched in aorta over other tissues and the IVC.…”

A aorta, o tecido elástico e a necrose cística da média

“…Cliff [8] suggested that an expansion occurs up to 20% of the diameter of the inner portions and 1% to 4% of the outer portions, although a change of only 10% of radial motion has been proposed [9]. Dobrin [10] reported that the descending thoracic aorta increases longitudinally 1%, while the ascending aorta and pulmonary artery increased from 5 to 11% [11].…”