Cardiac muscle (heart muscle) is one of the three major types of muscle, the others being skeletal and smooth muscle. It is an involuntary, striated muscle that is found in the walls of the heart. This muscle tissue is known as myocardium, and forms a thick middle layer between the outer layer of the heart wall (the epicardium) and the inner layer (the endocardium). Myocardium is composed of individual heart muscle cells (cardiomyocytes) joined together by intercalated disks, encased by collagen fibres and other substances forming the extracellular matrix.
Cardiac muscle contracts in a similar manner to skeletal muscle, albeit with some important differences. An electrical stimulation in the form of an action potential triggers the release of calcium from the cell's internal calcium store, the sarcoplasmic reticulum. The rise in calcium causes the cell's myofilaments to slide past each other in a process called excitation contraction coupling.
Diseases of heart muscle are of major importance. These include conditions caused by a restricted blood supply to the muscle including angina pectoris and myocardial infarction, and other heart muscle disease known as cardiomyopathies.
Video Cardiac muscle
Structure
Gross anatomy
Cardiac muscle tissue or myocardium forms the bulk of the heart. The heart wall is a three layered structure with a thick layer of myocardium sandwiched between the inner endocardium and the outer epicardium (also known as the visceral pericardium). The inner endocardium lines the cardiac chambers, covers the cardiac valves, and joins with the endothelium that lines the blood vessels that connect to the heart. On the outer aspect of the myocardium is the epicardium which forms part of the pericardium, the sack that surrounds, protects, and lubricates the heart. Within the myocardium there are several sheets of cardiac muscle cells or cardiomyocytes. The sheets of muscle that wrap around the left ventricle closest to the endocardium are oriented perpendicularly to those closest to the epicardium. When these sheets contract in a coordinated manner they allow the ventricle to squeeze in several direction simultaneously - longitudinally (becoming shorter from apex to base), circumferentially (becoming narrower from side to side), and with a twisting motion to squeeze out the maximum amount of blood with each heartbeat.
Striation
Cardiac muscle has cross striations formed by rotating segments of thick and thin protein filaments. Like skeletal muscle, the primary structural proteins of cardiac muscle are myosin and actin. The actin filaments are thin, causing the lighter appearance of the I bands in striated muscle, whereas the myosin filament is thicker, lending a darker appearance to the alternating A bands as observed with electron microscopy. However, in contrast to skeletal muscle, cardiac muscle cells are typically branch-like instead of linear.
T-tubules
Another histological difference between cardiac muscle and skeletal muscle is that the T-tubules in the cardiac muscle are bigger and wider and track laterally to the Z-discs. There are fewer T-tubules in comparison with skeletal muscle. The diad is a structure in the cardiac myocyte located at the sarcomere Z-line. It is composed of a single T-tubule paired with a terminal cisterna of the sarcoplasmic reticulum. The diad plays an important role in excitation-contraction coupling by juxtaposing an inlet for the action potential near a source of Ca2+ ions. This way, the wave of depolarization can be coupled to calcium-mediated cardiac muscle contraction via the sliding filament mechanism. Cardiac muscle forms these instead of the triads formed between the sarcoplasmic reticulum in skeletal muscle and T-tubules. T-tubules play critical role in excitation-contraction coupling (ECC). Recently, the action potentials of T-tubules were recorded optically by Guixue Bu et al.
Intercalated discs
The cardiac syncytium is a network of cardiomyocytes connected to each other by intercalated discs that enable the rapid transmission of electrical impulses through the network, enabling the syncytium to act in a coordinated contraction of the myocardium. There is an atrial syncytium and a ventricular syncytium that are connected by cardiac connection fibres. Electrical resistance through intercalated discs is very low, thus allowing free diffusion of ions. The ease of ion movement along cardiac muscle fibers axes is such that action potentials are able to travel from one cardiac muscle cell to the next, facing only slight resistance. Each syncytium obeys the all or none law.
Intercalated discs are complex adhering structures that connect the single cardiomyocytes to an electrochemical syncytium (in contrast to the skeletal muscle, which becomes a multicellular syncytium during mammalian embryonic development). The discs are responsible mainly for force transmission during muscle contraction. Intercalated discs consist of three different types of cell-cell junctions: the actin filament anchoring adherens junctions, the intermediate filament anchoring desmosomes, and gap junctions. They allow action potentials to spread between cardiac cells by permitting the passage of ions between cells, producing depolarization of the heart muscle. However, novel molecular biological and comprehensive studies unequivocally showed that intercalated discs consist for the most part of mixed-type adhering junctions named area composita (pl. areae compositae) representing an amalgamation of typical desmosomal and fascia adhaerens proteins (in contrast to various epithelia). The authors discuss the high importance of these findings for the understanding of inherited cardiomyopathies (such as arrhythmogenic right ventricular cardiomyopathy).
Under light microscopy, intercalated discs appear as thin, typically dark-staining lines dividing adjacent cardiac muscle cells. The intercalated discs run perpendicular to the direction of muscle fibers. Under electron microscopy, an intercalated disc's path appears more complex. At low magnification, this may appear as a convoluted electron dense structure overlying the location of the obscured Z-line. At high magnification, the intercalated disc's path appears even more convoluted, with both longitudinal and transverse areas appearing in longitudinal section.
Maps Cardiac muscle
Physiology
The physiology of cardiac muscle shares many similarities with that of skeletal muscle. The primary function of both muscle types is to contract, and in both cases a contraction begins with a characteristic flow of ions across the cell membrane known as an action potential. The action potential subsequently triggers muscle contraction by increasing the concentration of calcium within the cytosol.
However, the mechanism by which calcium concentrations within the cytosol rise differ between skeletal and cardiac muscle. In cardiac muscle, the action potential comprises an inward flow of both sodium and calcium ions. The flow of sodium ions is rapid but very short-lived, while the flow of calcium is sustained and gives the plateau phase characteristic of cardiac muscle action potentials. The comparatively small flow of calcium through the L-type calcium channels triggers a much larger release of calcium from the sarcoplasmic reticulum in a phenomenon known as calcium-induced calcium release. In contrast, in skeletal muscle, minimal calcium flows into the cell during action potential and instead the sarcoplasmic reticulum in these cells is directly coupled to the surface membrane. This difference can be illustrated by the observation that cardiac muscle fibres require calcium to be present in the solution surrounding the cell in order to contract, while skeletal muscle fibres will contract without extracellular calcium.
During contraction of a cardiac muscle cell, the long protein myofilaments oriented along the length of the slide over each other in what is known as the sliding filament hypothesis. There are two kinds of myofilaments, thick filaments composed of the protein myosin, and thin filaments composed of the proteins actin, troponin and tropomyosin. As the thick and thin filaments slide past each other the cell becomes shorter and fatter. In a mechanism known as crossbridge cycling, calcium ions bind to the protein troponin, which along with tropomyosin then uncover key binding sites on actin. Myosin, in the thick filament, can then bind to actin, pulling the thick filaments along the thin filaments. When the concentration of calcium within the cell falls, troponin and tropomyosin once again cover the binding sites on actin, causing the cell to relax.
Regeneration
Until recently, it was commonly believed that cardiac muscle cells could not be regenerated. However, a study reported in the April 3, 2009 issue of Science contradicts that belief. Olaf Bergmann and his colleagues at the Karolinska Institute in Stockholm tested samples of heart muscle from people born before 1955 who had very little cardiac muscle around their heart, many showing with disabilities from this abnormality. By using DNA samples from many hearts, the researchers estimated that a 4-year-old renews about 20% of heart muscle cells per year, and about 69 percent of the heart muscle cells of a 50-year-old were generated after he or she was born.
One way that cardiomyocyte regeneration occurs is through the division of pre-existing cardiomyocytes during the normal aging process. The division process of pre-existing cardiomyocytes has also been shown to increase in areas adjacent to sites of myocardial injury. In addition, certain growth factors promote the self-renewal of endogenous cardiomyocytes and cardiac stem cells. For example, insulin-like growth factor 1, hepatocyte growth factor, and high-mobility group protein B1 increase cardiac stem cell migration to the affected area, as well as the proliferation and survival of these cells. Some members of the fibroblast growth factor family also induce cell-cycle re-entry of small cardiomyocytes. Vascular endothelial growth factor also plays an important role in the recruitment of native cardiac cells to an infarct site in addition to its angiogenic effect.
Based on the natural role of stem cells in cardiomyocyte regeneration, researchers and clinicians are increasingly interested in using these cells to induce regeneration of damaged tissue. Various stem cell lineages have been shown to be able to differentiate into cardiomyocytes, including bone marrow stem cells. For example, in one study, researchers transplanted bone marrow cells, which included a population of stem cells, adjacent to an infarct site in a mouse model. Nine days after surgery, the researchers found a new band of regenerating myocardium. However, this regeneration was not observed when the injected population of cells was devoid of stem cells, which strongly suggests that it was the stem cell population that contributed to the myocardium regeneration. Other clinical trials have shown that autologous bone marrow cell transplants delivered via the infarct-related artery decreases the infarct area compared to patients not given the cell therapy.
Differences between atria and ventricles
Cardiac muscle forms both the atria and the ventricles of the heart. Although this muscle tissue is very similar between cardiac chambers, some differences exist. The myocardium found in the ventricles is thick to allow forcefull contractions, while the myocardium in the atria is much thinner. The individual myocytes that make up the myocardium also differ between cardiac chambers. Ventricular cardiomyocytes are longer and wider, with a denser T-tubule network. Although the fundamental mechanisms of calcium handling are similar between ventricular and atrial cardiomyocytes, the calcium transient is smaller and decays more rapidly in atrial myocytes, with a corresponding increase in calcium buffering capacity. The complement of ion channels differs between chambers, leading to longer action potential durations and effective refractory periods in the ventricles. Certain ion currents such as IK(UR) are highly specific to atrial cardiomyocytes, making them a potential target for treatments for atrial fibrillation.
Clinical significance
Diseases affecting cardiac muscle are of immense clinical significance, and are the leading cause of death in developed nations. The most common condition affecting cardiac muscle is ischaemic heart disease, in which the blood supply to the heart is reduced. In ischaemic heart disease, the coronary arteries become narrowed by atherosclerosis. If these narrowings gradually become severe enough to partially restrict blood flow, the syndrome of angina pectoris may occur. This typically causes chest pain during exertion that is relieved by rest. If a coronary artery suddenly becomes very narrowed or completed blocked, interrupting or severely reducing blood flow, a myocardial infarction or heart attack occurs. If the occlusion is not relieved promptly by medication, percutaneous coronary intervention, or surgery, then a region of heart muscle may become permanently scarred and damaged.
Heart muscle may become damaged despite a normal blood supply. The heart muscle may become inflamed in a condition called myocarditis, most commonly by viruses but sometimes by the body's own immune system. Heart muscle can also be damaged by drugs such as alcohol, long standing high blood pressure or hypertension, or persistent abnormal heart racing. Specific diseases of heart muscle called cardiomyopathies can cause heart muscle to become abnormally thick (hypertrophic cardiomyopathy), abnormally large (dilated cardiomyopathy), or abnormally stiff (restrictive cardiomyopathy). Some of these conditions are caused by genetic mutations and can be inherited.
Many of these conditions, if severe enough, can damage the heart so much that the pumping function of the heart is reduced. If the heart is no longer able to pump enough blood to meet the body's needs, this is described as heart failure.
See also
- Frank-Starling law of the heart
- Regional function of the heart
- Nebulette
References
External links
- Cardiac muscle histology
Source of the article : Wikipedia
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