Biomedical Engineering Reference
In-Depth Information
power of the vessel radius. Thus, a small decrease in radius will greatly increase
the resistance. The arterial resistance, a response to changes that mainly reside in
the distal arteries, can be caused by a number of factors associated with structural,
mechanical, and functional properties of the arterial wall. PVR, blood pressure,
and flow are all related; an increase in blood flow or a decrease in pressure in the
small arteries will result in a decrease in resistance, whereas a decrease in blood
flow or an increase in pressure results in an increase in resistance. Increased PVR
could be caused by pruning, vasoconstriction, or medial hypertrophy.
Pruning is a process in which there is a reduction in the total number of small
peripheral arteries. Pruning of the peripheral arteries may be paired with dilation of
the proximal arteries, resulting from constriction of the muscular arteries in
response to increased pressure [ 29 ]. Pruning is a structural change that may
increase vascular resistance in vascular diseases such as pulmonary hypertension
[ 30 ]. The increase in resistance is due to the loss of pathways through which the
blood can flow.
Vasoconstriction, or the decrease in blood vessel diameter, also contributes to
increases in PVR. Vasoconstriction involves the contraction of SMC due to
changes in environmental factors. For example, the elevation of calcium in pul-
monary SMCs leads to pulmonary vasoconstriction [ 31 ]. As the SMCs constrict,
the diameter of the small artery lumen will decrease, thus increasing the resistance
in the arteries. Hypoxic vasoconstriction develops to maintain the local ventila-
tion-perfusion relationship; this allows blood to be diverted from hypoxic regions
to regions with proper ventilation [ 32 ]. However, chronic hypoxia will lead to
narrowing of the arteries through muscularization and SMC proliferation, resulting
in an increase in PVR related to vasoconstriction. Vasoconstriction is controlled
through the production and release of mediators of vascular tone.
Medial hypertrophy involves the thickening of the arterial medial layer and leads
to the narrowing of the vascular lumen, which causes a greater resistance to flow.
This is the main contributor to increased PVR in pulmonary hypertension [ 28 ].
Medial hypertrophy can be caused by a number of different factors including,
recruitment of other cells, SMC hypertrophy, SMC proliferation and fibroblast cell
migration (Fig. 3 ). Endothelial cell dysfunction can cause the release of paracine
factors, such as growth factors, to induce SMC proliferation, or chemokines to
recruit circulating inflammatory cells [ 33 ]. The circulating inflammatory cells that
infiltrate the media are primarily composed of monocytes and macrophages. These
circulating cells attach to the endothelium and are able to penetrate into the vascular
wall increasing the medial thickness thus increasing PVR [ 34 ]. Fibroblasts
migrating to the medial layer may also contribute to medial hypertrophy. The
transdifferentiation, induced by environmental factors, of fibroblasts to myofibro-
blasts is a key aspect in vascular remodeling. Once transformed, myofibroblasts are
able to migrate from the adventitia to the media. Growth of the media can also result
from an increase in SMC size, or number, or both. Increased pressure in the small
arteries can cause SMC to undergo morphological and functional changes. Medial
thickening can change SMC from a contractile to a proliferative phenotype, where
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