Myocardial cells

Electrophysiological Experiments. Guinea pig myocardial cells prepared as described previously 24) were superfused at 37 C with a Tyrode solution. Electrical properties of the myocytes were examined by the patch-clamp methods (25) using fire-polished pipettes. The current was measured by means of a patch-clamp amplifier, stored on the tape through a digital PCM data recording system, and analyzed with a computer. 

Figure 5. Effect of maitotoxin (MTX) on the contractile activity of cultured rat myocardial cells. The value (mean of three sets of experiments) is the percentage of arrhythmically beating myocytes among total moving cells (43-69 myocytes). MTX concentration used...

Figure 6. Effect of maitotoxin (MTX, 3 x 10 g/mL) on the beating rate of cultured rat myocardial cells in the absence ( ) or presence (o) of verapamil (10 M). Verapamil was administered 5 min before the application of MTX, Vertical lines indicate the standard error of mean (n=5). (Reproduced with permission from Ref. 20. Copyright 1987 Elsevier)...

Tachycardia and increased contractility (due to SNS activation) Increase cardiac output Increased MV02 Shortened diastolic filling time P,-Receptor down-regulation, decreased receptor sensitivity Precipitation of ventricular arrhythmias Increased risk of myocardial cell death... 

Direct current cardioversion is the process of administering a synchronized electrical shock to the chest. The purpose of DCC is to simultaneously depolarize all of the myocardial cells, resulting in interruption and termination of the multiple reentrant circuits and restoration of normal sinus rhythm. The initial energy level of the shock is 100 joules (J) if the DCC attempt is unsuccessful, successive cardioversion attempts maybe made at 200,300, and 360 J.14 Delivery of the shock is synchronized to the ECG by the cardioverter machine, such that the electrical charge is not delivered during... 

Direct current cardioversion The process of administering a synchronized electrical shock to the chest to simultaneously depolarize all of the myocardial cells, resulting in restoration of normal sinus rhythm. 

Troponins T or I Proteins found predominantly in cardiac muscle that regulate calcium-mediated interaction of actin and myosin troponins I and T are released into the blood from myocytes at the time of myocardial cell necrosis after infarction. These biochemical markers become elevated and are used in the diagnosis of myocardial infarction. 

A 1,5-hour inhalation exposure of mixed breed rabbits to airborne concentrations of 72 ppm of hydrogen sulfide resulted in ventricular repolarization, while a 5-day, 0.5-hour/day exposure to this concentration resulted in cardiac arrhythmia (Kosmider et al. 1967). Histochemical staining of the myocardial cells revealed a reduction in adenosine tri-phosphate (ATP) phosphohydrolase and NADPH2 oxidoreductase (Kosmider et al. 1967). Cardiac arrhythmia, suggestive of a stimulus transmission disorder, was... 

Procainamide (Class IA antiarrhythmic drug) is an effective agent for ventricular tachycardia. Its mechanism of action involves blockade of the fast Na+ channels responsible for phase 0 in the fast response tissue of the ventricles. Therefore, its effect is most pronounced in the Purkinje fibers. The effects of this drug s activity include a decrease in excitability of myocardial cells and in conduction velocity. Therefore, a decrease in the rate of the phase 0 upstroke and a prolonged repolarization are observed. As a result, duration of the action potential and the associated refractory period is prolonged and the heart rate is reduced. These effects are illustrated by an increase in the duration of the QRS complex. 

Changes in heart rate also affect the contractility of the heart. As heart rate increases, so does ventricular contractility. The mechanism of this effect involves the gradual increase of intracellular calcium. When the electrical impulse stimulates the myocardial cell, permeability to calcium is increased and calcium enters the cell, allowing it to contract. Between beats, the calcium is removed from the intracellular fluid and the muscle relaxes. When heart rate is increased, periods of calcium influx occur more frequently and time for calcium removal is reduced. The net effect is an increase in intracellular calcium, an increased number of crossbridges cycling, and an increase in tension development. 

Atrial natriuretic peptide (ANP) released from myocardial cells in the atria of the heart inhibits the reabsorption of sodium from the collecting duct. The mechanisms of action of ANP include ... 

Atrial natriuretic peptide is released from myocardial cells in the atria of the heart in response to an increase in atrial filling, or an increase in plasma volume. This hormone inhibits the release of renin. With less angiotensin Il-induced vasoconstriction of the afferent arteriole, RBF, GFR, and urine output increase. The increased loss of water and solutes decreases blood volume toward normal. 

More recently, the clavulones (not specified which ones) [134] were described to have potent effects on the spontaneous beating rate of cultured myocardial cells from fetal mouse hearts. At a concentration of 0.45 pM, clavulone had positive chronotropic action on these cells however, the character of this effect clearly differed from the positive ionotropic and negative chronotropic effects of the steroid glycoside ouabain or the drug Bay K 8644. Hence, these results suggest that the clavulones may possess a new mechanism of action in this assay system. 

Biochemical markers of myocardial cell death are important for confirming the diagnosis of MI. An evolving MI is defined as a typical rise and gradual fall in troponin I or T or a more rapid rise and fall of CK-MB (Fig. 5-2). Typically, blood is obtained immediately and two additional times in... 

The shortage of donor hearts has prompted development of new surgical techniques, including ventricular aneurysm resection, mitral valve repair, and myocardial cell transplantation, which have resulted in variable degrees of symptomatic improvement. 

The mechanism of action of these drugs is not completely understood. However, it is very likely that they inhibit cellular phosphodiesterase of the myocardium, which leads to an elevation in the cellular level of cyclic AMP, which in turn facihtates contraction of myocardial cells. It is clear that these drags are not 8-adrenoreceptor antagonists, and that their effect is not mediated by inhibition of (Na -K+) ATPase. They simultaneously increase the flow of calcium ions into the cell. They are used for short-term control of patients that inadequately react to cardiac glycosides, diuretics, and coronary vasodilating agents. 

This can be accomplished either by reducing the load on the heart, or by lowering systemic venous and arterial pressure (nitrates and nitrites), or by partial suppression of adrenergic innervation of the heart (j3-adrenoreceptors), or by suppressing calcium ion transport in myocardial cells since the contraction of smooth muscles vessels is controlled by the concentration of calcinm ions in the cytoplasm (Ca channel blockers). The resulting effect of the aforementioned drngs is that they reduce the need for oxygen in the heart. 

Pharmacology Amiodarone possesses electrophysiologic characteristics of all 4 Vaughan Williams Classes but has predominantly Class III antiarrhythmic effects. The antiarrhythmic effect may be due to at least 2 major properties Prolongation of the myocardial cell-action potential duration and refractory period, and noncompetitive - and -adrenergic inhibition. 

Gold HK, Vacant JP, Oesterle SN. Percutaneous transvenous cellular cardiomyoplasty. A novel nonsurgical approach for myocardial cell transplantation. J Am Coll Card/o/2003 41 1964-1971. 

Within 3-4 hours of a heart attack, damaged myocardial cells release CK of the MB type, which can be detected In serum by a monoclonal antibody and Is useful to confirm the diagnosis. 

Cardiac glycosides display positive inotropic activity by a direct effect on the myocardial cells, trig-... 

Fig. 6. Influences of different types of antiarrhythmic agents (Vaughan-William s classification) on the shape of cardiac action potentials. First row Class I-agents action potentials of ventricular myocardial cells. Second row (from left to right) Action potential of SA-node cells influence of a )0-hlocker (class II). Action potential of ventricular myocardial cells influence of a class Ill-antiarrhythmic. Action potential of AV nodal cells influence of a class IV-antiarrhythmic (verapamil, diltiazem).

The drugs in class IC produce a marked depression in the rate of rise of the membrane action potential and have minimal effects on the duration of membrane action potential and ERP of ventricular myocardial cells. 

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