The intrinsic spontaneous contraction or beat of cardiac muscle is evident in embryonic cardiac muscle cells as well as in cardiac muscle cells in tissue culture. The heartbeat is initiated, locally regulated, and coordinated by specialized, modified cardiac muscle cells called cardiac conducting cells (Plate 25, page 348). These cells are organized into nodes and highly specialized conducting fibers called Purkinje fibers that generate and rapidly transmit the contractile impulse to various parts of the myocardium in a precise sequence. Both parasympathetic and sympathetic nerve fibers terminate in the nodes. Sympathetic stimulation accelerates the heartbeat by increasing the frequency of impulses to the cardiac conducting cells. Parasympathetic stimulation slows down the heartbeat by decreasing the frequency of the impulses. The impulses carried by these nerves do not initiate  contraction but only modify the rate of intrinsic cardiac muscle contraction by their effect at the nodes. The structure and functions of the conducting system of the heart are described in Chapter 13, Cardiovascular System.
A localized injury to cardiac muscle tissue that results in the death of cells is repaired by replacement with fibrous connective tissue. Consequently, cardiac function is lost at the site of injury. This pattern of injury and repair is seen in nonfatal myocardial infarction (MI). Confirmation of suspected MI in the individual can be made through the detection of specific markers in the blood. These markers are the structural  subunits TnI and TnT of the cardiac troponin complex. They are usually released into the bloodstream within 3 to 12 hours after an MI. TnI levels remain elevated for up to 2 weeks from the time of the initial injury; thus, it is regarded as an excellent marker for diagnosing MI that has recently occurred.
Mature cardiac muscle cells are able to divide.
In the past, it was thought that once cardiac muscle cells are destroyed, they cannot be replaced by new muscle cells. Recent studies of hearts removed from individuals who had received transplants reveal nuclei undergoing mitosis. Although the number of dividing nuclei in these hearts is low (0.1%), it suggests that damaged cells can potentially be replaced.  Perhaps in the future, a method might be developed that could induce human cardiac muscle to regenerate into healthy tissue.
Smooth muscle generally occurs as bundles or sheets of elongated fusiform cells with finely tapered ends (Fig. 11.18 and Plate 26, page 350). The cells, also called fibers, range in length from 20 m in the walls of small blood vessels to about 200 m in the wall of the intestine; they may be as large as 500 m in the wall of the uterus during pregnancy. Smooth muscle cells are interconnected by gap junctions, the specialized communication junctions between the cells (Fig. 11.19). Small molecules or ions can pass from cell to cell via these junctions and provide communication links that regulate contraction of the entire bundle or sheet of smooth  muscle.
Smooth muscle cytoplasm stains rather evenly with eosin in routine H&E preparations because of the concentrations of actin and myosin that these cells contain. The nuclei of smooth muscle cells are located in the center of the cell and often have a corkscrew appearance in longitudinal section. This characteristic is a result of contraction of the cell during fixation and is often useful in distinguishing smooth muscle cells from fibroblasts in routine histologic sections. In the noncontracted cell, the nucleus appears as an elongated structure with tapering ends, lying in the center axis of the cell. When the nucleus is included in a cross section of a smooth muscle fiber, it appears as a round or circular profile whether the cell is contracted or relaxed. The TEM shows that most of