Biomedical Engineering Reference
In-Depth Information
neighboring cardiac myocytes fuse at structures termed intercalated discs, which are typi-
cally present only along the longitudinal cell direction and not along the transverse direc-
tion (the intercalated discs are depicted as heavy black dashed lines penetrating the fibers
in Figure 4.2 ). Many gap junctions are present in the intercalated discs allowing for a rapid
communication between neighboring cardiac muscle cells. These gap junctions effectively
reduce the intercellular resistance to ion transfer, by at least two orders of magnitude, as
compared with ion movement across a cell membrane. Thus, there is a preference for com-
munication molecules (e.g., ions) to move in the longitudinal direction to rapidly pass
from one cardiac muscle cell to another cardiac muscle cell.
Although the physiology of cardiac muscle is quite different from skeletal muscle, car-
diac muscle contracts in a very similar way to skeletal muscle. Again, readers may be
familiar with this from a previous physiology course. Cardiac muscle fibers are striated
and composed of similar sarcomere structures as skeletal muscles. Actin and myosin
cross-bridges produce the necessary connections to allow for muscle contraction. These
proteins in the cardiac muscle unit are regulated with a very similar system to the troponin/
tropomyosin system in skeletal muscles, which requires increased intracellular calcium to
free actin binding sites. Again, similar to skeletal muscles, an action potential instigates
contraction in cardiac muscle cells. Due to the presence of the intercalated discs (with
many gap junctions) the action potential spreads from one cardiac myocyte to the neigh-
boring myocytes with almost no impediment to the speed of the signal. This allows the
formation of a muscle syncytium, which can work and produce contractions at the same
time.
The coupling between excitation of the cardiac myocytes and the contraction of the
muscle fibers is dictated by changes in the cell's cytosolic calcium concentration. Calcium
is released from the sarcoplasmic reticulum and then binds to troponin, which allows
the actin-myosin cross-bridge formation to begin. The major difference between cardiac
excitation-contraction coupling and skeletal excitation-contraction coupling is through the
presence of voltage-gated calcium channels within the T-tubule system of cardiac muscle
cells (the T-tubules are cytoplasmic invaginations that bring the extracellular space close to
the critical intracellular calcium compartments, like the sarcoplasmic reticulum). The open-
ing of these voltage-gated calcium channels causes a small increase in the intracellular cal-
cium concentration. This small increase allows for excess calcium to bind to calcium
receptors present on the sarcoplasmic reticulum membrane. Upon activation of these recep-
tors, calcium channels open to allow for the large movement of calcium ions out from the
sarcoplasmic reticulum into the intracellular space. This process is termed calcium-induced
calcium release, and this is a process that is not seen during skeletal muscle contraction.
The atrial and the ventricular myocytes compose two separate syncytiums in the heart.
When the atrial syncytium contracts as a whole, blood is ejected from the left and the right
atrium into the left and right ventricle, respectively. When the ventricular syncytium con-
tracts as a whole, blood is ejected from the two ventricles into the systemic or pulmonary
circulatory systems. These two syncytiums are separated by a fibrous tissue, which has a
very high electrical resistance associated with it. The high-resistance tissue prevents the
action potential signal from passing between the atria and the ventricles. Therefore, this
prevents the ventricles from contracting at the same time as the atria and allows atrial con-
traction to fully fill the ventricles with blood. To couple atrial contraction with ventricular
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