Biomedical Engineering Reference
In-Depth Information
Fig. 3
Cell
recruitment,
fibroblast
migration,
and
SMC
proliferation
and
hypertrophy
all
contribute medial hypertrophy
abnormal cell growth dominates [
35
]. SMC hypertrophy accounts for the increase
in SMC mass thickening of the medial layer in hypertension [
36
].
4 Arterial Wall Mechanical Stresses
Endothelial cells live in mechanically active environments, and experience stress
and strain in both physiological and pathological conditions. The biomechanical
stress imposed on cells in vivo is manifested as a complex multi-axial stress, often
including various anisotropic biaxial stress conditions. The artery wall continually
adapts to the changing mechanical environment, due to growth, remodeling, repair,
and disease. Therefore, the structure undergoes irreversible changes due to blood
flow. Blood vessels are subjected to mechanical forces of hydraulic pressure,
circumferential stretch, and shear stress due to the pulsatile nature of blood flow.
Blood pressure (BP) determines the amount of mechanical stretch on a vessel; BP
creates radial, normal, and tangential, or shear, forces on the vessel wall. Normal
stresses on the vessel wall affect all layers, the intima, media, and adventitia, while
shear stress only directly affect the layer that it is in contact with the blood flow,
the endothelial cells of the intima (Fig.
4
).
Blood pressure is a major determinant of vessel stretch; it creates radial and
tangential forces on the blood vessel wall that affect all cells types (Fig.
4
).
Arterial stretch or strain is the radial distension and longitudinal elongation of the
vessel which are caused by changes in pressure and flow of the blood. Strain is
defined as e
ΒΌ
Dr
=
r
or the ratio of the change in radius of the vessel to the original
radius of vessel before pressure application. Circumferential strains on the wall are
very
complex,
but
can
be
estimated
from
measurement
of
blood
pressure,
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