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V S Markhasin

Publications and source records attributed to V S Markhasin.

At least 37 records · Page 2Linked to original sources
PubMed1989

[The effect of asynchronous contraction of the myocardium on its mechanical function].

The effect of asynchronous excitation of adjacent portions of intact myocardium was simulated in two parallel connected papillary muscles from the rabbit heart right ventricle. Mechanical characteristics (length-force, force-rate, final systolic length-specific time of relaxation) of each of the muscles were recorded in simultaneous and asynchronous contractions. The asynchronism was found to exert a positive inotropic effect in each of the muscles and a negative one in the duplex. The asynchronism decelerated the temporal course of relaxation both in separate muscles and in duplex. The asynchronism-related mechanochemical dissociation seems to be the crucial phenomenon underlying the whole cycle of the mechanical phenomena.

Animals↗
PubMed1987

[Mechanism of postextrasystolic potentiation of the myocardium].

Combined effects of poststimulation and postextrasystolic potentiation (PESP) were studied in the rat papillary muscles. The constant PESP augmentation of isometric force triggered by extrasystolic stimulus was shown for 2-8 poststimulatory potentiated contractions. The PESP was not dependent upon the Ca2+ concentration within the 0.5-1.2 mM range. The findings corroborate the postulate that the PESP in cardiomyocytes is associated with special Ca2+ store which is triggered by two APs: regular and extrasystolic ones.

Animals↗
PubMed1987

[Effect of the anti-arrhythmia compounds etmozin and ethacizine on the contractile activity of myocardial preparations from heart defect patients].

Changes in contraction amplitudes, contraction peak time and relaxation time were evaluated at 50% and 80% of contraction peak, with adrenaline or strophanthin acting on the myocardium pretreated with antiarrhythmic substances, using atrial specimens from patients with acquired heart diseases and septal defects. Etmozin and ethacizine were shown to have a negative inotropic effect, reducing contraction intensity by about 50%. Adrenaline and strophanthin are capable of restoring myocardial contractility in the presence of antiarrhythmic effects without actually inducing spontaneous auto-arrhythmic activity. Causes of the recovery of myocardial mechanical activity, effectuated by adrenaline or strophanthin in the presence of antiarrhythmic agents are discussed. It is suggested that a combination of effective antiarrhythmic properties and negative inotropic effect of phenothiazines is significant for cases of arrhythmias with and without signs of heart failure.

Anti-Arrhythmia Agents↗
PubMed1987

[Effect of stretching on the action potentials of the human and rabbit ventricular myocardium].

The effect of stretching from L0 to Lmax on the electrical activity was studied on human myocardial preparations from patients with heart disease and on strips of rabbit ventricular myocardium. Muscular deformation was shown to decrease the amplitude and velocity of depolarization in slow action potentials. The action potentials (AP) possessing a fast depolarization phase were not sensitive to physiological stretching. Antiarrhythmic drugs--ethmozin (2 X 10(-5) M) and ethacizin (2 X 10(-6) M)--caused a decrease in the rate of AP depolarization, thus increasing AP sensitivity to deformation. It is suggested that stretching under the action of ethmozin and ethacizin reduced cardiomyocyte excitability due to suppression of slow Ca-current.

Action Potentials↗
PubMed1984

[Adrenaline-induced autorhythmic activity in the isolated atrial myocardium of mitral stenosis patients and its suppression by etmozin and ethacizin (the diethylamino analog of etmozin)].

The authors studied the effect of the new Soviet antiarrhythmic phenothiazine drugs etmozine and etacizine (a diethylamine analog of etmozine) on the adrenaline-induced (10(-4)M) autorhythmic activity of the myocardium of the atria of patients with mitral stenosis. Different types of autorhythmic activity occurring in the myocytes of the atria of patients with mitral stenosis are described. It was established that neither etmozine nor etacizine produce any significant changes in the action potential (AP) amplitude and in the maximal diastolic potential of spontaneous AP. However, the action of etacizine on the rate of diastolic depolarization and the frequency of AP discharges was more remarkable. Moreover, etacizine (10(-5) g/ml) completely suppressed autorhythmic activity of the myocytes in 60% of the preparations whereas etmozine administered at the same concentration only in 33%. It is assumed that substantially higher efficacy of etacizine in the reduction of the adrenaline-induced autorhythmic activity in human atrial fibers as compared with etmozine is explained by the action of etacizine not only on the fast sodium current but also on the slow calcium current.

Action Potentials↗
PubMed1982

[Effect of stretch of the electric activity of human myocardial cells].

The effects of cyclic deformation (0.03-0.3 mm/S) on electrical activity was examined on an isolated myocardium of patients suffering from mitral stenosis and congenital septal heart diseases. The muscle deformation was shown to decrease prepotential (the first component) and spike (the second component) amplitudes of double component action potentials which were specific for the pathological myocardium under study. It was also found that appearance of the second component was delayed in the course of deformation and almost ceased after deformation reached certain level. The delay of appearance of the second component was followed by the emergence of the second twitch that was similar to the extrasystolic one. Disappearance of the second component produced a decrease in contractility. When action potentials recorded were typical of the normal myocardium, they manifested no changes even upon a significant stretch. It is suggested that high sensitivity to stretch of the double component action potentials depends on conduction disturbances seen in the pathological myocardium.

Action Potentials↗
PubMed1981

[Kinetics of myocardial isometric relaxation in patients with congenital and acquired heart defects].

The kinetics of isometric relaxation was examined in an isolated myocardium of patients undergoing surgical correction of mitral stenosis (MS), congenital septal heart defects (SHD) and on papillary muscles (PM) of patients suffering from mitral valvular insufficiency. The relaxation of MS preparations is slower than that of SHD that manifests in the decrease of the characteristic constants K and alpha. PM relaxation is slower than that of the rabbit ventricular muscle. Adrenaline and the increased stimulation rate accelerate the relaxation of the preparations of all groups (the greatest increase is seen in MS). Verapamil and paired stimulation slow down the constants. It is suggested that the action potential duration influences the relaxation constants in PM and MS preparations but not SHD. The constants in question seem likely to be independent of the myocardial inotropic state.

Electric Stimulation↗
PubMed1981

[Effect of paired stimulation on the electrical and mechanical activity of myocardial cells in congenital and acquired heart defects].

Thin myocardial strips were dissected from the papillary muscles of patients undergoing mitral valve replacement (group I) and atrial tissue of patients undergoing the correction of congenital septal defects (group II) and mitral stenosis (group III). Electrical activity and isometric tension were measured. Paired stimulation (PS) with time intervals of 250-350 ms and 380-440 ms activated two action potentials (AP) for each potentiated contraction (80 and 70% of force increase, respectively) in bundles of groups I and III. Strips of group III had depressed level of resting potential (RP) and different types of AP including AP with additional spike activity in the plateau phase. The inotropic effect of PS depends on the level of the resting potential. If RP was more than 45 mv PS activated two AP or one doubled AP for each potentiated contraction (80-120% of force increase). If RP was less than 35 mv PS was not able to initiate doubled AP and to initiate the increase of contractility. Epinephrine (10(-6) g/ml) increased the depressed RP and AP in group III bundles and potentiated the inotropic effect of PS in groups I and III. Verapamil (2 X 10(-6) g/ml) inactivated the doubled AP and abolished the inotropic effect of PS in group III strips. It is supposed that additional inflow of Ca during excitation produces the inotropic effect of paired stimulation in human myocardium.

Action Potentials↗
PubMed1978

[Contractile reaction of the myocardium of patients with heart diseases to chemical scarification of cell membranes].

Strips of the myocardium from the auricula atria of patients suffering from mitral stenosis (MS) and septal defects of the heart (SDH) removed during the operation were treated with ethylenediaminetetraacetic acid (DETA)--3mM--to increase the cell membrane permeability (scarification). The mechanical response of the contractile proteins to the change in the Ca2+ was recorded in the ethylene-hexaaminetetraacetic acid (EHTA)--3mM--against the background of increased membrane permeability to the Ca-EHTA complex permitting to regulate Ca2+ concentration in myofibrillae from 10(-9) to 10(-4)M. As shown, with the same threshold concentrations (5.10(-8)M) and saturation concentrations (10(-4)M) of Ca2+ the strips from the patients with MS developed the maximal tension per cross section unit of the strip half as great as the preparations from patients with SDH, this indicating a possible affection of the contractile proteins in the hearts of patients with MS. The ratio between the tension amplitudes under conditions of a complete calcium activation of the contractile proteins and a single isometric contraction for the preparations obtained from the patients with MS was 8 to 10, and with SDH--from 4 to 5. It is supposed that this was the result of more pronounced changes in the apparatus of electromechanical conjugation of the myocardium of patients suffering from MS.

Calcium↗
PubMedDate not supplied

Mechano-electric interactions in heterogeneous myocardium: development of fundamental experimental and theoretical models.

The heart is structurally and functionally a highly non-homogenous organ, yet its main function as a pump can only be achieved by the co-ordinated contraction of millions of ventricular cells. This apparent contradiction gives rise to the hypothesis that 'well-organised' inhomogeneity may be a pre-requisite for normal cardiac function. Here, we present a set of novel experimental and theoretical tools for the study of this concept. Heterogeneity, in its most condensed form, can be simulated using two individually controlled, mechanically interacting elements (duplex). We have developed and characterised three different types of duplexes: (i) biological duplex, consisting of two individually perfused biological samples (like thin papillary muscles or a trabeculae), (ii) virtual duplex, made-up of two interacting mathematical models of cardiac muscle, and (iii) hybrid duplex, containing a biological sample that interacts in real-time with a virtual muscle. In all three duplex types, in-series or in-parallel mechanical interaction of elements can be studied during externally isotonic, externally isometric, and auxotonic modes of contraction and relaxation. Duplex models, therefore, mimic (patho-)physiological mechano-electric interactions in heterogeneous myocardium at the multicellular level, and in an environment that allows one to control mechanical, electrical and pharmacological parameters. Results obtained using the duplex method show that: (i) contractile elements in heterogeneous myocardium are not 'independent' generators of tension/shortening, as their ino- and lusitropic characteristics change dynamically during mechanical interaction-potentially matching microscopic contractility to macroscopic demand, (ii) mechanical heterogeneity contributes differently to action potential duration (APD) changes, depending on whether mechanical coupling of elements is in-parallel or in-series, which may play a role in mechanical tuning of distant tissue regions, (iii) electro-mechanical activity of mechanically interacting contractile elements is affected by their activation sequence, which may optimise myocardial performance by smoothing intrinsic differences in APD. In conclusion, we present a novel set of tools for the experimental and theoretical investigation of cardiac mechano-electric interactions in healthy and/or diseased heterogeneous myocardium, which allows for the testing of previously inaccessible concepts.

Animals↗
PubMedDate not supplied

[Mathematical model of a generalized calcium buffer in cardiac muscle cells].

The problem of reduction of the earlier model for the calcium buffer system of cardiomyocytes was solved. A simpler model of generalized buffer, was obtained, which reproduces the behavior of the initial system in typical situations. To identify the parameters of the equations of the generalized buffer, recursive algorithms of filtration were developed. The model consists of two equations, which describe separately the fast and slow components of the buffer system. It is shown that the error of the generalized buffer model relative to the initial model of the calcium buffer system does not exceed 10% in a wide range of Ca2+ transients. The introduction of the generalized buffer into the model of mechanochemical coupling provides a more realistic description of a decrease in free calcium concentration. The new model adequately describes all mechanical events simulated by the initial model. In terms of the model, the effect of the slow component of the generalized buffer in a single contraction-relaxation cycle was studied. It was shown that the presence of the slow component leads to a marked decrease in the amplitude of contraction and increase in relaxation time.

Buffers↗
PubMedDate not supplied

[Experimental-theoretical study of the force-interval relationship in the developing chicken myocardium].

The force-interval relationship was studied on myocardium preparations from chick embryos and hatched chickens. It is shown that the force-interval relationships of myocardium change during ontogenesis. A negative staircase (a decrease in the isometric force with increasing stimulation rate) in the chick embryo myocardium and a positive steady-state relationship in hatched stage myocardium were revealed. Changes in the force after switching from one stimulation frequency to another, the effects of poststimulation potentiation, as well as responses to the introduction of pauses and extrasystols at a constant stimulation rate were recorded. All the effects observed in the transient processes in preparations from hatched stage myocardium were more pronounced than in embryo myocardium. Our previous mathematical model of calcium recirculation in cardiomyocytes was adapted for simulating the main features of force-interval relationships in embryonal and relatively developed myocardium. The main source of regulatory calcium in the model of hatched stage myocardium is sarcoplasmic reticulum. In the model of embryo myocardium, it was postulated, based on data available in literature, that the main regulator of contractile response of the muscle is calcium that enters cardiomyocytes from extracellular medium. To describe force-interval relationships, by this model, the decreasing dependence of the entry of extracellular calcium on the intervals between stimuli was introduced.

Animals↗