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Mechanism of cardiac muscle contraction

The main contractile proteins of myocardial cells are actin and myosin (Fig. 30).

In the state of polarization (rest) long filaments of actin lie separately from filaments of myosin. A polarized cell has on its external membrane a positive charge and on the internal one — negative charge.

When an impulse in the form of acetylcholine comes up to the cellular membrane from conduction system of the heart, the properties of membrane are changed. It becomes permeable for Na⁺ to penetrate the cells and for K⁺ to go out of the cells. Sodium, as is known, becomes electrically neutral inside the cell. In order to create electric neutrality of the cell calcium comes out from Ca⁺⁺ depot — sarcoplasmic reticulum, and contributes to linking into a complex of actin with myosin, and activates ATP, breaking it down to ADP and AMP.

Chemical energy of degradation is being transformed into mechanical one by means of binding actin and myosin through calcium — so-called troposinic complex with the use of AMP energy. As a result a contraction of the cell occurs. At this moment, depolarization of membrane ceases, the properties of membrane are sharply changed: K⁺ returns from interstitial space into the cell, Na leaves the cell. Calcium under the influence of altered relations between K⁺ and Na⁺returns into sarcoplasmic reticulum. A repolarization of membrane starts, actin-myosin complex is degraded. Degradation of actin-myosin complex also needs in energy of AMP that is already being generated by splitting ATP with the help of Mg⁺⁺.

The extracellular calcium is also of significance for cardiac muscle contraction. Hypocalcemia may be the cause of cardiac muscle weakness.

Thus, a terminal link of different forms of cardiac insufficiency is the disturbance of Ca⁺⁺ transport in the cells of cardiac muscle. Calcium is a peculiar "conductor" of cardiac activity. Resynthesis of ATP occurs in mitochondria of the cell by aerobic way. In hypoxia ATP resynthesis occurs by anaerobic way, but its synthesis decreases 18 times, since a depletion of ATP stores takes place in cardiac muscle. In the cells of conduction system ATP resynthesis occurs under anaerobic conditions, therefore these cells are resistant to hypoxia.

The state of coronary blood circulation, a narrowing of the lumen of coronary arteries in particular, plays a great role in the origin of cardiac insufficiency. In those areas where a coronary blood flow is decreased a hypoxia of myocardium develops. This leads to anaerobic resynthesis of ATP with depletion of its stores, disturbance of Ca⁺⁺ transport to the actin-myosin complex and development of low myocardial contractility.

Hypokalemia, as well as hypocalcemia and hypomagnesemia, is the factor leading to myocardial insufficiency.

Causes of circulatory failure (according to Lang):

1. The overfatigue of cardiac muscle in patients with heart defects, myocardial hypertrophy.

2. A disturbance of blood supply of cardiac muscle (atherosclerosis, infarction).

3. Intoxications, directly influencing the myocardium (influenza, diphtheria, etc.).

4. Neurotrophic effects upon the myocardium. Catecholamines serve as the "lock" for a proper operation of the myocardium.

5. Hormonal influences on cardiac activity, for example, accumulation of adrenalin, lead to ATP degradation, disturbance of high-energy bonds and processes of power supply. The heart remains in the refractory period, changes over to anaerobic pathway of metabolism.

6. Combined causes producing a cardiac failure.

According to Heglv they distinguish hemodynamic (congestive) and energetic-dynamic failure.

In the basis of development of circulatory failure lies a decrease of myocardial metabolism, and after this the peripheral changes develop.

Basic principles of pharmacotherapy in coronary and myocardial insufficiency:

— an increase of oxygen and substrates of metabolism supply to cardiocytes and stimulation of ATP synthesis (oxygenotherapy, antiaggregates, thrombolytics, coronarodilatators, adrenomimetics, glucose-insulin-calium mixture);

— a decrease of energy consumption (antihypoxants, antioxidants, calcium antagonists, blockers of phospholipase and lipase activities, membrane-stabilizing agents — glucocorticoids, nonsteroid hormones);

— a protection of mechanisms of synthesis, transport and ATP utilization.
Usually, the acute right ventricular failure and acute left ventricular failure

are distinguished.

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