Structural and architectural changes during arterial development and the role of hemodynamics.
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.
Stehbens
W E
WE
Department of Pathology, Wellington School of Medicine, New Zealand.
D000818:Animals; D001011:Aorta / Q000033:anatomy & histology* / Q000196:embryology / Q000502:physiology; D002455:Cell Division; D004730:Endothelium, Vascular / Q000166:cytology / Q000196:embryology / Q000502:physiology; D005260:Female; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D009131:Muscle, Smooth, Vascular / Q000502:physiology; D011247:Pregnancy; D013314:Stress, Mechanical; D017539:Tunica Intima / Q000166:cytology / Q000196:embryology / Q000502:physiology