Biomedical subjects
V G Shevchuk
Publications and source records attributed to V G Shevchuk.
[The hypertensive reactions during endothelin exposure on the structures of the ventrolateral medulla oblongata].
Administration of endothelin induced a hypertensive response in anesthetised cats. The mechanism of this response seems to involve an augmentation of the resistance of peripheral vessels due to enhanced descending sympatho-activating influences.
[Caffeine eliminates the positive inotropic effect of paired stimulation in the myocardium of warm-blooded animals].
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[Structural effects in the sarcolemma of the cardiomyocytes under the action of modulators of the polyphosphoinositide system].
The influence of activators (Ca(2+)-channels stimulator BAY K 8644 and phospholipase C stimulator fMLP) and inhibitors (Ca(2+)-channels blocker verapamil and alpha 1-adrenoceptors blocker prazosin) of the polyphosphoinositide system on cardiomyocytes sarcolemma, was studied. The structural effects of the PPI modifiers seem to be one of the mechanisms of the PPI physiological activity at the membrane level.
[The effect of polyfunctional macroheterocycles on the rhythmic and contractile activity of the myocardium in animals].
The effect of the polyfunctional macroheterocycles on the rhythmic and contractile activity of the rat myocardium was found to depend on their concentration. A two-phasic effect upon contractility of the papillary muscles was revealed: a short-term (up to 20 sec) positive inotropic effect followed by a stable depression. The most active drug of this class, dicyclohexano-18-crown-6, prevented the positive inotropic action of classic stimulants (catecholamines and strophantin) upon the contractile function of the heart.
Contractile function and Ca2+ transport system of myocardium in ageing.
Experiments with animals with various species-specific life span (rats, rabbits, cats, dogs) and different models (in situ heart, isolated perfused heart, isolated papillary muscle) have proved the reduction of functional capacity of the ageing heart. Diversely directional age-dependent shifts have been established involving myocardial Ca2+ transport system, i.e. an increase in the rate of Na+-Ca2+ exchange and passive Ca2+ transport across sarcolemma and a decrease in its Ca2+-binding capacity and a decrease in Ca2+ accumulation by sarcoplasmic reticulum and mitochondria (Ca2+ uptake). The experiments revealed a decrease in the Ca2+ ATPase myosin activity in the myocardium of aged animals and absence of age changes in the K+ ATPase activity. The findings obtained suggest that the development in the cardiac contractile function disorders in ageing largely depends on the age-related changes in the Ca2+ transport system.
[The contractile function and calcium-transport system of the myocardium in aging].
Experiments with different species of animals and different models (in situ heart, isolated perfused heart, isolated papillary muscle) revealed a reduction of functional capacity of ageing heart. A decrease of Ca2+ uptake by sarcoplasmic reticulum and mitochondria and diverse age-dependent shifts were found in sarcolemma. The data obtained suggest that the development of the cardiac contractile function disorders in ageing largely depends of the age-related changes in the Ca2+ transport system.
Antioxidants as antiarrhythmic drugs.
Experiments on rats and rabbits using models of arrhythmias induced by vasopressin, epinephrine, strophanthin, and CaCl2 showed that antioxidants derived from 1,4-dihydropyridines, dibunol, and alpha-tocopherol possessed antiarrhythmic effects. Administration of these antioxidants decreased the occurrence of extrasystoles, disturbances of atrioventricular conductivity and ventricular fibrillation. These drugs also prevented changes in membrane phospholipid composition, inhibited activation of peroxidation, decreased phospholipase activity, prevented a decrease of Ca2+ ATPase and Ca2+ binding and uptake by sarcoplasmic reticulum, and increased sarcolemmal Na+, K+-ATPase, sarcoplasmic reticulum creatine phosphokinase.
[Adrenergic and cholinergic regulation of the tonus of coronary vessels in old dogs].
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The effect of hormones on the haemodynamics in animals of different age groups.
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[Hormonal regulation of the heart in aging].
It was established in experiments on adult (8--12 month) and old (26--32 month) rats that in ageing the sensitivity of the cardiovascular system to certain hormones--adrenaline, vasopressin, insulin, thyroxine, estradiol dipropionate--grows while its reactivity to them diminishes. The administration of these hormones causes significant changes in hemodynamics and myocardial contractility. Adrenaline and thyroxine lead to an increase in the blood minute and stroke volume, arterial pressure, cardiac index and left ventricular work index, maximum rate of intraventricular pressure growth, maximum rate of myocardial fiber shortening, and in the contrastility index. Vasopressin and insulin cause a decrease in the indices of general hemodynamics. The increased sensitivity of the heart to hormones at old age and diminution of its reactivity lead to prolonged, protracted reactions of the cardiovascular system in elderly and old individuals.
Experimental analysis of development of cardiac insufficiency in old age.
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[Nervous regulation of cardiac function during aging].
The hemodynamic changes and myocardium contractile capacity following the extracardiac nerves stimulation with acetylcholine, norepinephrine, inderal, regitin and atropine, as well as the activity of main enzymes of cholinergic and adrenergic metabolism, were studied in albino rats, rabbits, and cats of various age. With ageing, the thresholds of vagal and sympathetic nerves influences on the heart increased, the sensitivity of heart to acetylcholine and norepinephrine changed. In old animals, smaller atropine and in deral doses blocked the respective cholinergic and beta-adrenergic reactions. Alterations of transmitters metabolism play an important role in the mechanism of age-induced changes in nervous control of cardiac function.
[Role of protein biosynthesis activation in the mechanism of the negative chronotropic action of the vagus nerve and acetylcholine on the heart].
In rats, the following data were obtained: a) acetylcholine activates the rate of protein biosynthesis in auricles in vitro; b) protein biosynthesis inhibitors (actinomycine D, sarcolysine, neutral rot, tolluidine blue) weaken the negative chronotropic effect of acetylcholine and vagus on the heart; c) anabolic hormones increase the cholinergic effect on heart; d) acetylcholine induces hyperpolarization of the myocardial fibers which is prevented by actinomycine D. The activation of protein biosynthesis followed by hyperpolarization of the pacemaker cells seems to play an important role in the mechanism of negative chronotropic effect of acetylcholine and vagus on the heart.
[Mechanisms of development of cardiac insufficiency in old age].
Tests conducted with adult (8--10 months) and old (26--28 months) rats brought evidence that in ageing the cardiac ejection, dp/dt max, contractility index, the ATP concentration, that of creatinophosphate, glycogen, pyruvate decline, the phosphorylation coefficient, the lactate content increase, while the level of water-soluble proteins and collagen diminishes and that of water-insoluble ones decreases. In adult rats hemodynamics and myocardial contractility change but unsignificantly on the 4--6th day after coarctation of the aorta, whereas in the old ones there occur functional and metabolic alterations in the heart that are indicative of a developing cardiac insufficiency. The age-specific differences persist also on the 14--16th day following coarctation of the aorta. During these periods the weight of the heart, the content of the myofribrillary proteins and collagen are on the rise, whereas in the old ones the weight of the heart remains unchanged and the level of water-soluble protein drops. Changes in the properties of the actomyosin complex, disruption of the calcium pump, shifts in the system of the energy generation, limitation of potential possibilities incident to the systems of protein biosynthesis in the myocardial cell, all this leads to the development of cardiac incompetence following loading in old age.
Hemodynamics and its regulation in old age.
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[Regulation of hemodynamics in old age].
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[Effect of acetylcholine and catecholamines on the hemodynamics at various stages of ontogenesis].
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