Cardiac muscle (heart muscle) is one of the three main types of muscles, the other is skeletal and smooth muscle. It is an unconscious gastric muscle that is found in the heart wall. This muscle tissue is known as myocardium , and forms a thick middle layer between the outer layers of the heart wall (epicardium) and the inner layer (endocardium). Myocardium is composed of individual heart muscle cells (cardiomyocytes) united by interrupted discs, enclosed by collagen fibers and other substances that form extracellular matrices.
The contraction of the heart muscle in a way similar to skeletal muscle, though with some important differences. Electrical stimulation in the form of action potential triggers the release of calcium from the cell's internal calcium store, the sarcoplasmic reticulum. The increase in calcium causes cell myofilaments to slide past each other in a process called excitation excitation clutch.
Heart muscle disease is very important. These include conditions caused by limited blood supply to muscles including angina pectoris and myocardial infarction, and other heart muscle disease known as cardiomyopathy.
Video Cardiac muscle
Struktur
Anatomi bruto
Cardiac muscle tissue or myocardium forms most of the heart. The heart wall is a three-layer structure with a thick layer of myocardium sandwiched between the inner endocardium and the outer epicardium (also known as the visceral pericardium). Inner endocardium coats the heart space, including the heart valves, and joins the endothelium lining the blood vessels connected to the heart. On the outside aspect the myocardium is the epicardium that forms part of the pericardium, the sack that surrounds, protects, and lubricates the heart. In the myocardium there are several sheets of cardiac muscle cells or cardiomyocytes. The muscle sheath that covers the left ventricle closest to the endocardium is oriented perpendicular to the one closest to the epicardium. When these sheets contract in a co-ordinated fashion they allow the ventricles to press in several directions simultaneously - longitudinally (being shorter from top to bottom), radially (narrower from side to side), and in a circular motion (similar to wringing a damp cloth) to squeeze the maximum amount of blood with each heartbeat.
Histology
When looking at it microscopically, the heart muscle can be likened to the wall of a house. Most of the walls are taken up by bricks, which in the heart muscle are the individual heart muscle cells or cardiomyocytes. The mortar that surrounds the brick is known as the extracellular matrix, produced by a support cell known as fibroblasts. In the same way that the walls of the house contain electrical wires and pipes, the heart muscle also contains special cells to perform electrical signals quickly (the heart conduction system), and the blood vessels to bring nutrients to the muscle cells and take the products- waste products (coronary arteries, veins and capillary tissue).
Cardiac muscle cells
The heart muscle cells or cardiomyocytes are the contracting cells that allow the heart to pump. Each cardiomyocyte needs to contract with the coordination of its neighboring cells to efficiently pump blood out of the heart, and if this coordination is damaged later - although individual cells contract - the heart may not pump at all, as can occur during abnormal heart rhythms such as ventricular fibrillation.
Seen through a microscope, the heart muscle cells are roughly rectangular, 100-150 in size? M with 30-40 m. Individual cardiac muscle cells join together at the end with an interspersed disk to form long fibers. Each cell contains myofibrils, a special protein fiber that shifts through each other. These are arranged in sarcomomes, the basic contractile units of muscle cells. Regular organization of myofibrils into sarcoma gives the heart muscle cells the appearance of striped or striated when viewed through a microscope, similar to skeletal muscle. These striations are caused by a mild band I consisting mainly of a protein called actin, and a darker band primarily composed of myosin.
Cardiomyocytes contain T-tubules, membrane pockets that flow from the surface to the cell's interior which helps to increase contraction efficiency. The majority of these cells contain only one nucleus (though they may have as many as four), unlike skeletal muscle cells that usually contain many nuclei. Heart muscle cells contain many mitochondria that provide the energy needed for cells in the form of adenosine triphosphate (ATP), making them highly resistant to fatigue.
T-tubules
T-tubules are microscopic tubes that travel from the cell surface into cells. They are continuous with the cell membrane, consisting of the same phospholipid bilayer, and exposed on the cell surface to the extracellular fluid that surrounds the cell. T-tubules in the heart muscle are larger and wider than skeletal muscle, but there are fewer numbers. In the center of the cell they join together, running into and along the cell as a transverse axial network. Inside their cells lie close to the internal calcium cell store, the sarcoplasmic reticulum. Here, a pair of single tubules with part of the sarcoplasmic reticulum are called cisternal terminals in a combination known as a dyad.
T tubular functions include rapid emitting electrical impulses known as the action potential from the cell surface to the cell nucleus, and help regulate the concentration of calcium in cells in a process known as excitation-contraction coupling.
Interconnected disk
The cardiac syncytium is a network of cardiomyocytes connected to each other by intercalated discs that allow the rapid transmission of electrical impulses through the tissues, allowing the syncytium to act in a coordinated contraction of the myocardium. There is syncytium atrium and ventricular syncytium linked by the heart connection fibers. The electrical resistance through the interspersed discs is very low, thus allowing the diffusion of ions freely. The ease of movement of ions along the axis of the heart muscle fibers is such that the action potential can travel from one cardiac muscle cell to the next, just facing little resistance. Each syncytium obeys all or all laws.
Cak intercalation is a complex inherent structure that connects a single cardiomyocyte to an electrochemical syncytium (in contrast to skeletal muscle, which becomes a multicellular syncytium during mammalian embryo development). Discs are responsible primarily for the transmission of force during muscle contraction. The interconnected disk consists of three different types of cellular connections: actin filaments interwoven junctional junctions, intermediate intermediate filaments of desmosomes, and junction gaps. They allow the potential for action to spread between the heart cells by allowing the passage of ions between the cells, resulting in cardiac muscle depolarization. However, the new comprehensive biological and molecular studies actually show that the intercalated disks consist of mostly mixed type mixed intersections called composita area area compositae ) represents a unique combination of desmosomal proteins and fascia adhaerens (in contrast to epithelials). The authors discussed the importance of these findings to understand the inherited cardiomyopathy (such as right ventricular arithmogenic cardiomyopathy).
Under a light microscope, the interspersed discs appear as thin lines, usually dark lines that divide the adjacent cardiac muscle cells. The interconnected disk runs perpendicular to the direction of the muscle fibers. Under an electron microscope, the interconnected disk paths appear more complex. At low magnification, this may appear to be a dense electron-dense structure above the obscured Z-line location. At high magnification, intercalated disc lines appear even more convoluted, with both longitudinal and transverse areas appearing in the longitudinal section.
Fibroblast
Cardiac fibroblasts are vital support cells in the heart muscle. They can not provide strong contractions such as cardiomyocytes, but are largely responsible for creating and maintaining the extracellular matrix that forms mortars in which embedded cardiomyocyte bricks. Fibroblasts play an important role in responding to injury, such as myocardial infarction. After injury, fibroblasts can become active and transform into myofibroblasts - cells that exhibit behavior somewhere between fibroblasts (producing extracellular matrix) and smooth muscle cells (contraction ability). In this capacity, fibroblasts can repair the injury by creating collagen while gently contracting to pull the edges of the injured area together.
Fibroblasts are smaller but more numerous than cardiomyocytes, and some fibroblasts may be attached to the cardiomyocyte at once. When attached to cardiomyocyte they can affect electric current through the cell's surface membrane of the muscle, and in a context called electrically coupled. Other potential roles for fibroblasts include electrical isolation from the cardiac conduction system, and the ability to transform into other cell types including cardiomyocytes and adipocytes.
Extracellular matrix
Continuing the analogy of the heart muscle as wall-like, the extracellular matrix is ​​the mortar that surrounds the cardiomyocyte and fibroblasts. This matrix consists of proteins such as collagen and elastin along with polysaccharides (sugar chains) known as glycosaminoglycans. Together, these substances provide support and strength for muscle cells, create elasticity in the heart muscle, and keep muscle cells hydrated by binding water molecules.
The matrix in direct contact with muscle cells is referred to as basal membrane, mainly composed of type IV collagen and laminin. Cardiomyocytes are associated with a basement membrane through a special glycoprotein called integrin.
Maps Cardiac muscle
Physiology
The physiology of heart muscle has much in common with skeletal muscle. The main function of both types of muscles is to contract, and in both cases the contractions begin with the typical ion stream across the cell membrane known as the action potential. The potential for subsequent action triggers muscle contraction by increasing the concentration of calcium in the cytosol.
However, the mechanism by which the calcium concentration in the cytosol increases is different between skeletal and cardiac muscle. In the heart muscle, the action potential consists of the inward flow of both sodium and calcium ions. The sodium ion stream is fast but very short, while the calcium flow is maintained and provides the phase characteristic of the potential plateau of heart muscle action. The relatively small calcium flow through the L-type calcium channel triggers a much greater calcium release 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 otherwise the sarcoplasmic reticulum in these cells is directly coupled to the surface membrane. This difference can be illustrated by the observation that the heart muscle fibers require calcium to be present in the solution around the cell to contract, while the skeletal muscle fibers will contract without extracellular calcium.
During the contraction of the heart muscle cells, long protein myofilaments oriented along the length of the slides on top of each other in what is known as the sliding filament hypothesis. There are two types of myofilaments, thick filaments consisting of myosin proteins, and thin filaments consisting of actin, troponin and tropomiosin proteins. As the thick, thin filaments slide past each other, the cells become shorter and fatter. In a mechanism known as crossbridge cycling, calcium ions bind to troponin proteins, which together with tropomiosin then reveal the key binding sites on actin. Myosin, in thick filaments, can bind to actin, attracting thick filaments along thin filaments. When the concentration of calcium in the cell drops, troponin and tropomyosin once again cover the binding sites on the actin, causing the cell to relax.
Regeneration
To date, it is generally believed that heart muscle cells can not be regenerated. However, a study reported in the April 3, 2009 edition of Science contradicts that belief. Olaf Bergmann and colleagues at the Karolinska Institute in Stockholm examined heart muscle samples from people born before 1955 who had very small heart muscle around their heart, many of which showed defects in this disorder. Using DNA samples from many livers, researchers estimate that a 4-year-old renews about 20 percent of heart muscle cells per year, and about 69 percent of 50-year-old heart muscle cells are produced after he or she is born.
One of the ways cardiomyocyte regeneration occurs is through the division of cardiomyocytes that already existed during the normal aging process. The process of division of existing cardiomyocytes has also been shown to increase in areas adjacent to the site of myocardial injury. In addition, certain growth factors promote self-renewal of endogenous cardiomyocytes and heart stem cells. For example, growth factors such as insulin 1, hepatocyte growth factor, and high mobility group B1 protein increase the migration of heart stem cells to the affected area, as well as the proliferation and viability of these cells. Some family members of the fibroblast growth factor also induce re-entry of small cardiomyocyte cells. The vascular endothelial growth factor also plays an important role in the recruitment of native heart cells to the infarct site in addition to its angiogenic effects.
Based on the natural role of stem cells in cardiomyocyte regeneration, researchers and clinicians are increasingly interested in using these cells to induce the regeneration of damaged tissues. Various lineages of stem cells have proven capable of differentiating 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 the location of the infarcts in the mouse model. Nine days after surgery, the researchers discovered a new band of myocardial regeneration. However, this regeneration is not observed when the injected cell population does not have stem cells, which strongly suggests that it is a stem cell population that contributes to myocardial regeneration. Other clinical trials have demonstrated that autologous marrow cell transplants are transmitted through infarct arteries associated with decreased infarction areas compared to patients not given cell therapy.
Difference between atria and ventricle
The heart muscle forms the atria and the heart's ventricles. Although these muscle tissues are very similar between heart chambers, some differences exist. The myocardium is found in the thick ventricle to allow for strong contractions, while the myocardium in the atrium is much thinner. Individual myocyte-forming myocardium also differs between heart chambers. Ventricular cardiomyocytes are longer and wider, with more dense T-tubule tissue. Although the basic mechanisms of calcium handling are similar between ventricular and atrial cardiomyocytes, the transient calcium is smaller and decays faster in the atrial myocytes, with an increase in the capacity of the appropriate calcium buffer. Complementary ion channels differ between rooms, leading to longer duration of action and an effective refractory period in the ventricles. Certain ion streams such as I K (UR) are very specific for atrial cardiomyocyte, making it a potential target for treatment for atrial fibrillation.
Clinical interests
Diseases affecting heart muscle have a very large clinical significance, and are the leading cause of death in developed countries. The most common condition that affects the heart muscle is ischemic heart disease, where the blood supply to the heart is reduced. In ischemic heart disease, the coronary arteries are narrowed by atherosclerosis. If this narrowing gradually becomes severe enough to limit some of the blood flow, angina pectoris syndrome may occur. This usually causes chest pain during exertion which is removed by rest. If the coronary arteries suddenly become very narrow or finished blocked, interfere or greatly reduce blood flow through the blood vessels, myocardial infarction or heart attack occurs. If the blockage does not immediately disappear with medication, percutaneous coronary intervention, or surgery, then the heart muscle area can become a permanent and damaged scar.
Cardiac muscle can also become damaged despite normal blood supply. The heart muscle can become inflamed under a condition called myocarditis, most commonly caused by a viral infection but occasionally caused by the body's own immune system. Cardiac muscle can also be damaged by drugs such as alcohol, high blood pressure or long-lasting hypertension, or persistent abnormal heartbeat. Specific heart muscle disease called cardiomyopathy can cause the heart muscle to become very thick (hypertrophic cardiomyopathy), abnormal (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 function of the heart pump is reduced. If the heart is no longer able to pump enough blood to meet the body's needs, it is described as heart failure.
See also
- Frank-Starling's law from the heart
- Regional function of the heart
- Nebulette
References
External links
- histology of the heart muscle
Source of the article : Wikipedia
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