Myocardial pacemaker cells

Myocardial infarction, 3 710-711 and blood coagulation, 4 81 Myocardial pacemaker cells, 5 81 Myocardium, 5 79—80 Myoglobin, properties of standard, 3 836t Myosin, role in heart excitation and contraction coupling, 5 81 Myrac aldehyde, 2 278 24 485 Myrascone, 24 571... 

The rhythm of heart contractions depends on many parameters condition of pacemaker cells and the conduction system, myocardial blood flow, and other factors consequently, arrhythmia can originate for different reasons that are caused by disruptions in electrical impulse generation or conduction. They can be caused by heart disease, myocardial ischemia, electrolytic and acid-base changes, heart innervation problems, intoxication of the organism, and so on. 

Calcium is involved in the contraction of cardiac and vascular smooth muscle cells, and in the auto-maticity of cardiac pacemaker cells. Actions of calcium channel blockers on vascular smooth muscle cells are described with the main account of these drugs in Chapter 23. Although the three classes of calcium channel blocker have similar effects on vascular smooth muscle in the arterial tree, their cardiac actions differ. The phenylalkylamine, verapamil, depresses myocardial contraction more than the others, and both verapamil and the benzothiazepine, diltiazem, slow conduction in the SA and AV nodes. 

Calcium channel blockers inhibit the passage of calcium through the membrane charmels the result in myocardial cells is to depress contractility, and in pacemaker cells to suppress their automatic activity. Members of the group therefore may have negative cardiac inotropic and chronotropic actions. These actions can be separated nifedipine, at therapeutic concentrations, acts almost exclusively on noncardiac ion charmels and has no clinically useful anti-arrhythmic activity whilst verapamil is a useful antiarrhythmic. 

The Tbxl8-induced automaticity could represent a new way to provide pace the heart. Thus, Tbxl8-mediated conversion of adult ventricular myocytes into pacemaker cells was examined in vivo. To accomplish this, an bi-cistronic adenoviral vector expressing Tbxl8 and eGFP was directly and focaUy injected into the heart apex in guinea-pigs. Direction intra-myocardial injection led to... 

As the graph below shows, the action potential curve for pacemaker cells, such as those in the sinoatrial node, differs from that of other myocardial cells. Pacemaker cells have a resting membrane potential of -60 mV (instead of -90 mV), and they begin to depolarize spontaneously. Called diastolic depolarization, this effect results primarily from calcium and sodium leakage into the cell. 

Tachyarrhythmias (sinus rate more than 100 per minute) are produced by a disturbances of impulse generation or of impulse conduction in the heart. Tachyarrhythmias due to disturbed impulse formation are associated with irregular and rhythmic discharge from ectopic pacemaker activity in areas of the heart other than the SA node. The characteristic of myocardial cells, which enables them to generate spontaneous depolarization, is called automaticity. 

Direct effects on the heart are determined largely by Bi receptors, although B2 and to a lesser extent a receptors are also involved, especially in heart failure. Beta-receptor activation results in increased calcium influx in cardiac cells. This has both electrical and mechanical consequences. Pacemaker activity—both normal (sinoatrial node) and abnormal (eg, Purkinje fibers)—is increased (positive chronotropic effect). Conduction velocity in the atrioventricular node is increased (positive dromotropic effect), and the refractory period is decreased. Intrinsic contractility is increased (positive inotropic effect), and relaxation is accelerated. As a result, the twitch response of isolated cardiac muscle is increased in tension but abbreviated in duration. In the intact heart, intraventricular pressure rises and falls more rapidly, and ejection time is decreased. These direct effects are easily demonstrated in the absence of reflexes evoked by changes in blood pressure, eg, in isolated myocardial preparations and in patients with ganglionic blockade. In the presence of normal reflex activity, the direct effects on heart rate may be dominated by a reflex response to blood pressure changes. Physiologic stimulation of the heart by catecholamines tends to increase coronary blood flow. 

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