[Changes in balance of ionic currents of cardiac cells as one of the mechanisms of arrhythmia].

Changes in balance of transmembrane ionic currents were achieved in two ways: 1) modifying Na current with lysophosphatidylcholine (LPC), a toxic metabolite of ischemia; 2) modifying Ca current with BAY K 8644, an agonist of Ca channels. Elementary current through Na channel were recorded in an inside-out mode using patch clamp techniques. The effects of BAY K 8644 were studied on the transmembrane potential of guinea pig papillary muscle (PM) and sheep Purkinje fibers (PF).

[Inotropic effect of chlorpromazine on the frog atrium].

The chlorpromazine, a calmodulin inhibitor, has been studied for its action on the contraction force and calcium current of the frog atrium fibres. Chlorpromazine (10(-5) mol/l) was observed to induce maximal increase of the contraction force that 30 min after the agent action amounted to (47.3 + 9.

[Effects of diltiazem and tetrodotoxin on the development of hypoxic contracture of the guinea pig myocardium].

In the isolated electrically stimulated right ventricular papillary muscles the onset of hypoxic contracture occurred 7 +/- 1.2 min and reached maximum 29.2 +/- 4.

[influence of Ca channel blockers on the positive inotropic effect of ionophore A23187 in the myocardium].

Calcium ionophore A23187 (10(-5) M) increases the force of contraction of the frog atrium up to 27 + 4.8%. The calcium antagonists d-600 (5 X 10- M), Zn2+ (2 X 10(-5) M), Mn2+ (2 X 10(-4) M) decrease the force of contraction 50, 10 and 20%, respectively, and inhibit the positive inotropic effect of ionophore A23187.

[Formation of ectopic excitation in the heart under the action of aconitine. II. The generation of oscillatory fluctuations of the membrane potential and current].

The method of potential fixation was used to study the mechanism of the origin of membrane potential oscillations induced by aconitine (50, 100 mg/l) on isolated trabeculae of Rana ridibunda atrium. Some of the sodium channels change their properties under the effect of aconitine: these channels are activated at potentials close to the rest potential, while the rate of their inactivation is slowed down. The direct cause of the aconitine ectopic excitation are oscillations of the sodium current caused by modified channels.

[Formation of ectopic stimulation in the heart under the action of aconitine. I. The dynamics of input and output membrane currents].

Rapid sodium and slow input and output currents were studied by the double saccharose bridge method on isolated atrial trabeculae of Rana ridibunda under the effect of aconitin (100 mg/l). It is shown that the ptroperties of rapid sodium channels change under the effect of aconitin. As the result of this, activation of the input sodium current begins at potentials which are close to the rest potential, the maximum value of sodium conduction reduces, while the reverse potential for sodium current is shifted in the direction of lower potentials.

[Effect of creatine phosphate on the slow inward calcium current, action potentials and the strength of myocardial contraction].

The effect of creatine phosphate on the frog heart muscle involved maintenance of its contraction at high level even after inhibition of mitochondrial oxidative phosphorylation by sodium cyanide. The effect of creatine phosphate on the contractile force and action potential is similar for the frog heart ventricle and atrium. The voltage--clamp technique showed that creatine phosphate controlled the slow inward calcium current through the surface membrane of the frog atrium cells.

[Action of a new antiarrhythmia preparation, etmozin, on the contractile force, transmembrane action potential and the rapid incoming sodium flow of the frog atrial muscle].

The mechanism of the effect of ethmosine on the force of contraction, the membrane potential and the rapid incoming sodium flow of the frog atrium was studied by means of microelectrode technique and the method of potential fixation. It has been shown that in a concentration of up to 10(-5) g/ml ethmosine reduces the rate of increase of the foremost front of the action potential by 50%; has no substantial effect on the force of contraction, and on the shape and duration of the transmembrane action potential; inhibits the rapid incoming sodium flow by more than 50% by diminishing maximum conductivity of sodium ions; has no effect on processes of activation, inactivation and reactivation of the sodium flow. A comparison is made between ethmosine and other antiarrhythmic agents in their effect on the force of contraction and the electric parameters of cardiac cells.