Biomedical Engineering Reference
In-Depth Information
As we have seen, the three primary cells within the arterial wall are the endothe-
lial cells in the intima , the smooth muscle cells in the media , and the fibroblasts
in the adventitia . The luminal surface of the endothelial has potent anticoagulant
function. This property of the endothelium is in contrast to, for example, the highly
thrombogenic character of the intramural type I and type III collagen. Clearly, then,
an important role of the endothelium is to act as a smooth, nonthrombogenic lin-
ing that separates the wall contents from the flowing blood. The endothelium allows
transport of substances to and from the bloodstream, however; hence, it must be con-
sidered as a selective barrier. Notwithstanding the importance of these functions of
an intact endothelium, it was long thought that these were its only two roles. It is
now known however that the endothelium is very active biologically: it can regu-
late coagulative processes, synthesize vasoactive substances (e.g., nitric oxide (NO)
and endothelin-1 (ET-1)), produce growth-regulatory molecules (e.g., vascular en-
dothelial growth factor (VEGF), platelet derived growth factor (PDGF), fibroblast
growth factor (FGF)), and synthesize connective tissue (e.g., type IV collagen and
proteoglycans). Moreover, many blood-borne vasoactive substances affect the arte-
rial wall only in the presence of an intact endothelium, thus it also serves as a chemo-
transducer. Conversely, many biological functions of the endothelium are signaled
mechanically as, for example, via changes in local blood flow and the associated
wall shear stress: increased flow downregulates the synthesis of the vasoconstrictor
ET-1 and upregulates that of the vasodilators like NO, thus resulting in a flow-related
vasodilation. Endothelial cells also tend to elongate and align themselves in the di-
rection of the blood flow, which thereby reorients their actin microfilaments and
alters cytoskeletal properties. Hence, although it is a small fraction of the arterial
wall, the endothelium plays a major role in vascular mechanics.
Smooth muscle cells comprise about 25 % to 60 % of the arterial wall by dry
weight. They can increas in size (i.e., hypertrophy) or increase in number via cell
division (i.e., hyperplasia) depending on the stimulus. Structurally, smooth muscle
cells contain a Ca 2 + regulated actin-myosin contractile apparatus, albeit not arranged
in sarcomeres as in striated muscles, and they can possess a well-developed Golgi
apparatus which enables the synthesis of connective tissue, a capability that is very
important during development but also plays a detrimental role in aging and different
pathologies. Note, too, that various signals are capable of changing the phenotype
of the mature smooth muscle cell from contractile to synthetic. Contraction of a
vascular smooth muscle occurs much more slowly than that of a striated muscle,
typically beginning 5 to 100 ms after the initial stimulus and taking on the order
of 1 to 10 seconds to achieve its maximum level. Nevertheless, smooth muscles can
maintain maximum contraction at a steady level for much longer periods than striated
muscle, provided a stimulus persists, and with less energy expenditure (perhaps as
little as 0.25 % to 5 % of the energy required for comparable contraction of skeletal
muscle). Indeed, this ability is essential in the maintenance of the basal tone.
Despite some differences, the general relations between the force, length, and ve-
locity of shortening are similar for smooth and striated muscle, both able to generate
an active muscle stress of about 0.3 MPa. Like skeletal muscle, smooth muscle gen-
erates its maximum force at a unique length (often denoted with L 0 ). That is, there
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