4.5 Article

Functional, mechanical and geometrical adaptation of the arterial wall of a non-axisymmetric artery in vitro

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JOURNAL OF HYPERTENSION
卷 22, 期 2, 页码 339-347

出版社

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00004872-200402000-00018

关键词

hemodynamics; vascular remodeling; in vitro culture; matrix metalloproteinase; scleroproteins

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Objective Vascular remodeling is an adaptive response to variations in the hemodynamic environment acting on the arterial wall. Remodeling translates into changes of structure, geometry and mechanical properties of the artery. Our aim was to study the remodeling response of pig right common carotid arteries in vitro. Methods In vivo right carotid arteries are exposed to a non-uniform hemodynamic environment and exhibit a strong wall asymmetry in the circumferential direction that allows the study of two regions separately, as the artery remodels under in vitro perfusion. Porcine right common carotid arteries were cultured during 1 day (n = 6), 3 days (n = 6) or 8 days (n = 6) in an in vitro organ culture system, at a constant perfusion pressure of 100 mmHg. Geometrical, histological, biomechanical and biological analysis of the perfused segments was performed at the end of each study. Results Smooth muscle cell nuclei density and wall thickness remain constant along the culture periods. Elastin and collagen are significantly redistributed to equilibrate their relative content along the vessel circumference. The distensibility profile is significantly different at day 8. Matrix metalloproteinase-2 expression and activity increase significantly at days 3 and 8. Conclusion The non-axisymmetric arterial wall adapts to a uniform hemodynamic environment by redistributing the structural components of the extracellular matrix. The changes of collagen and elastin density may result from a vascular remodeling process involving matrix metalloproteinase-2 up-regulation and enzymatic activity. The remodeling response results in a new vascular wall configuration that is more distensible at physiological pressures (30-120 mmHg) and stiffer at higher pressures. (C) 2004 Lippincott Williams Wilkins.

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