Tuesday 18 November 2003
They are arranged largely in a circumferential and spiral orientation around the left ventricle, the chamber that pumps blood to the systemic circulation.
Cardiac myocytes have five major components:
(1) cell membrane (sarcolemma) and T-tubules, for impulse conduction
(2) sarcoplasmic reticulum, a calcium reservoir needed for contraction
(3) contractile elements
Cardiac muscle cells contain many more mitochondria between myofibrils than do skeletal muscle cells (approximately 23% of cell volume vs. 2%), reflecting the almost complete dependence of cardiac muscle on aerobic metabolism. Cardiac muscle cells each usually contain one spindle-shaped nucleus. Ventricular muscle contracts during systole and relaxes during diastole.
The functional intracellular contractile unit of cardiac muscle (like skeletal muscle) is the sarcomere, an orderly arrangement of thick filaments composed principally of myosin, and thin filaments containing actin.
Sarcomeres also contain the regulatory proteins troponin and tropomyosin. Cardiac muscle cells are composed of many parallel myofilaments (arrays of sarcomeres in series), which are responsible for the striated appearance of these cells.
Contraction of cardiac muscle occurs by the cumulative effort of sliding of the actin filaments between the myosin filaments toward the center of each sarcomere.
The lengths of sarcomeres range from 1.6 to 2.2 μm, depending on the state of contraction. Shorter sarcomeres have considerable overlap of actin and myosin filaments, with consequent reduction in contractile force, whereas longer lengths enhance contractility (Frank-Starling mechanism).
Thus, moderate ventricular dilation during diastole increases the subsequent force of contraction during systole. With progressive dilation, however, there is a point at which effective overlap of the actin and myosin filaments is reduced, and the force of contraction turns sharply downward, as occurs in heart failure.
The myocytes comprise only approximately 25% of the total number of cells in the heart. However, because cardiac myocytes are so much larger than the intervening cells, they account for more than 90% of the volume of the myocardium.
The remainder are endothelial cells, mostly associated with the rich myocardial capillary network, and fibroblasts. Inflammatory cells are rare and collagen is sparse in normal myocardium.
Reflecting their different functional requirements, atrial myocytes are generally smaller in diameter and less structured than their ventricular counterparts.
Some atrial cells also differ from ventricular cells in having distinctive electron-dense granules in the cytoplasm called specific atrial granules.
They are the sites of storage of atrial natriuretic peptide (ANP, or A-type natriuretic peptide), a polypeptide secreted into the blood under conditions of atrial distention. ANP can produce a variety of physiologic effects, including vasodilation, natriuresis, and diuresis, actions beneficial in pathologic states such as hypertension and congestive heart failure.
Other natriuretic peptides are produced by the ventricles in response to elevations of ventricular pressure and volume (B-type, initially called brain natriuretic peptide) and by the vascular endothelium (C-type) in response to elevated shear stress.
Functional integration of myocytes is mediated by structures unique to cardiac muscle called intercalated disks, which join individual cells and within which specialized intercellular junctions permit both mechanical and electrical (ionic) coupling.
One of the components of intercalated disks are gap junctions, which facilitate synchronous myocyte contraction by providing electrical coupling with relatively unrestricted passage of ions across the membranes of adjoining cells. Gap junctions consist of clusters of plasma membrane channels that directly link the cytoplasmic compartments of neighboring cells.
Abnormalities in the spatial distribution of gap junctions and their respective proteins in ischemic and myocardial heart disease may contribute to electromechanical dysfunction (arrhythmias).
In addition, specialized excitatory and conducting myocytes within the cardiac conduction system are involved in regulating the rate and rhythm of the heart.
(1) the sinoatrial (SA) pacemaker of the heart, the SA node, located near the junction of the right atrial appendage with the superior vena cava;
(2) the atrioventricular (AV) node, located in the right atrium along the atrial septum;
(3) the bundle of His, which courses from the right atrium to the summit of the ventricular septum; and its division into
(4) right and left bundle branches that further arborize in the respective ventricles.
PAS in cardiomyocytes
< object width="425" height="350"> < param name="movie" value="http://www.youtube.com/v/EdS_W22EnAI"> < /param> < param name="wmode" value="transparent"> < /param> < embed src="http://www.youtube.com/v/EdS_W22EnAI" type="application/x-shockwave-flash" wmode="transparent" width="425" height="350"> < /embed> < /object>
Anversa P, Nadal-Ginard B: Myocyte renewal and ventricular remodeling. Nature 415:240, 2002.