[The nature of pacemaker activity]. / O prirode peismekernoi aktivnosti.

A general equation of the membrane resting potential (RP) has been derived for closed cell membrane (CM) model. It is shown that Na,K-ATPase of cardiomyocytes is in the antielectrogenic phase. A hypothesis is proposed: a pacemaker cell is an excitable cell, which has RP corresponding to the given activity of Na,K-ATPase and non-activated cationic conductivities of CM higher than the activation threshold of Na-channels. The equation of the equipotential levels of the membrane RP on the surface of the cationic conductivities has been derived. It is shown that the substances (e. g. neuromediator) that change the membrane cation permeability are able to depolarize or to hyperpolarize CM. The direction of polarization is dependent on the state of the cell electrogenic system. The following factors promote the hyperpolarizing effect of the magnifying cation permeability substances: 1) high activity of Na,K-ATPase, 2) low background cation permeability of CM (among their number the integrity of CM) and 3) high ratio of the potassium permeability alteration in respect to that of sodium which is evoked by the substance (delta gK/delta gNa).

[Potassium transport in ischemia and anoxia of the perfused liver]. / Transport kaliia pri ishemii i anoksii perfuziruemoi pecheni.

It is theoretically explained and experimentally shown that the hepatocyte loss of potassium during total liver ischemia is much smaller than under the conditions of anoxia with volume velocity of perfusion remaining constant.

[Analysis of an equivalent electric circuit of the hepatocyte during stopping and restoration of the blood flow]. / Analiz ékvivalentnoi élektricheskoi skhemy gepatotsita v usloviiakh prekrashcheniia i vosstanovleniia krovotoka.

An analysis of an electric scheme of hepatocyte under conditions of stopping and restoring the blood flow taking into account the morphological and biochemical characteristics of the normal and injured liver was carried out. It is shown that the fast phase of restoring the membrane potential (MP) when restoring the blood flow following ischemia is stipulated by restoring extracellular concentrations of potential-generating ions; and slow restoring of the normal liver MP is connected with the phase of potassium efflux hyperpolarization. The injured liver MP stability to ischemia is higher because of the transmembrane ion gradient decrease before ischemia and next effect of depolarisation of passive currents weakening under conditions of closed extracellular space, and total ATPase activity decrease, i.e. a more economical ATP expenditure by the cell at ischemia.

[Hyperpolarization of the cell membrane during Na,K-ATPase inactivation]. / Giperpoliarizatsiia kletochnoi membrany pri inaktivatsii Na,K-ATFazy.

The relationship equation between the resting potential and potassium and sodium active currents is deduced in terms of a generally accepted model of electrogenesis. It is demonstrated that an increase of Na,K-ATPase activity to the estimated magnitude results in hyperpolarization of the cell membrane (CM), but the subsequent increase of the activity led to CM depolarisation. CM depolarisation results in an increase of the cell volume.

[Morphobiophysical parallels in assessing the hepatotropic action of nitrosodimethylamine]. / Morfobiofizicheskie paralleli pri otsenke gepatotropnogo deistviia nitrozodimetilamina.

On the third day after a single administration of nitrosodimethylamine (30 mg/kg) to white rats histochemistry reveals the greatest injury to the liver parenchyma. This correlates with a reduction in relative strength of intercellular contacts, an increase in relative strength of the membranes, and an elevation of the membrane potential during liver tissue survival in vitro. The latter fact can be explained, at any rate partially, by the lowering of the activity of cytoplasmic ATPase which competes with electrogenic Na+. K+-ATPase for ATP.

[Stability of the membrane potential of mouse liver cells to damaging exposures]. / Ustoichivost' membrannogo potentsiala kletok pecheni myshei pri povrezhdaiushchikh vozdeistviiakh.

Behavior of the membrane potential under some experimental effects changing the stability of liver electrogenesis was studied. A method for evaluating the stability of electrogenesis and some possible mechanisms of stabilization of the membrane potential at standard damage of the tissue is analysed.