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Biomedical subjects

F Z Meerson

Publications and source records attributed to F Z Meerson.

At least 163 records · Page 9Linked to original sources
PubMed1987

[Prevention of a stress-induced drop in the threshold of cardiac fibrillation using transauricular electroacupuncture].

The effect of electroacupuncture on stress-induced drop in cardiac fibrillation threshold and catecholamine content in the adrenergic terminals of the myocardium was studied in Wistar rats. Transauricular electroacupuncture causing drowsiness in animals was found to prevent a drop in cardiac fibrillation and norepinephrine level in the adrenergic terminals usually observed after long immobilization stress. It is assumed that the preventive effect of acupuncture may be attributable to reflex activation of the inhibitory brain system which restricts stress reaction.

Acupuncture Therapy↗
PubMed1987

[Stress-limiting systems and the problem of the prevention of arrhythmia].

Marked systemic resistance to damaging effects of stress develops as a result of repeated short-term stress exposures. This kind of adaptation is ensured by the activation of stress-limiting systems, namely, the opioidergic, GABA-ergic, serotoninergic, as well as antioxidant and prostaglandin ones. Proceeding from the stress-limiting system concept, adaptation to repeated stress exposure, as well as metabolites, synthetic analogues and activators of stress-limiting systems were successfully used to prevent and eliminate cardiac arrhythmias and fibrillations associated with acute ischemia, myocardial infarction and postinfarction cardiosclerosis. Prospects of further studies of stress-limiting systems' metabolites and activators as antiarrhythmic agents are considered.

Adaptation, Physiological↗
PubMed1987

[Increased enzymatic activity of antioxidant protection of the heart in the adaptation of rats to short-term stress exposure].

It has been shown that adaptation to short-term emotional-painful stresses leads to an increase in antioxidant enzyme activities but does not change vitamin E content in the myocardium. The most labile enzyme was catalase (35% increase). During stress in nonadapted animals the enzyme activity decreased, as compared to the control, while in the group of adapted animals with subsequent stress the activity was even higher than in the control. During initiation of lipid peroxidation in the heart homogenates in vitro there was a 3-fold increase and a 1%-fold decrease in the oxidation intensity in rats exposed to stress and in adapted animals, respectively. The role of adaptation activation of cardiac antioxidant system in the prevention of stress-induced heart damage is discussed.

Adaptation, Physiological↗
PubMed1987

[Effect of stress and the antioxidant ionol on the biosynthesis of catecholamines and the content of dopamine in the heart and adrenal glands].

The effects of a synthetic antioxidant ionol (dibunol) on the biosynthesis and content of catecholamines in the heart and adrenal glands were studied. It was shown that in stress a mobilization of catecholamine reserve is combined with a considerable increase in dopamine concentration. In conditions of physiological rest, ionol did not affect the studied indices of adrenal catecholamine biosynthesis, while in the heart it enhanced the dopamine synthesis and content. With ionol administration, stress did not suppress but, on the contrary, increased the neuronal uptake and noradrenaline biosynthesis, catecholamine concentration remaining practically unchanged. Simultaneously, a manyfold increase in the biosynthesis along with a considerable increase in the concentration of dopamine developed in both organs. The data obtained suggest that ionol realizes its stress-defensive effect to a great extent due to the activation of catecholamine biosynthesis and to a concomitant increase in dopamine accumulation.

Adrenal Glands↗
PubMed1986

[Effect of stress on the cardiomyocyte transmembrane potential of the working heart and its recovery after hypothermia].

Emotional-painful stress in rats was shown to decrease insignificantly transmembrane cardiomyocyte potential (TCP) measured in isolated hearts. The recovery of TCP following its depression due to the preparation cooling was twice slower in stress-exposed than in control animals. This is in keeping with the data on stress-induced disturbances of Na, K-ATPase activity (an enzyme playing a leading role in TCP maintenance). It is suggested that the disturbance in cation pump function activity plays a certain role in the onset of arrhythmias and cardiac fibrillation during stress.

Animals↗
PubMed1986

[Prevention of stress-induced disorders of myocardial Na, K-ATPase activity using adaptation to short-term stress].

It was shown that adaptation to short-term emotional-painful stresses prevented both the decline in the activity and the increase in thermal denaturation rate of Na,K-ATPase in sarcolemmal vesicles isolated from the rat myocardium exposed to prolonged stress. The role of Na-pump damage in the disturbance of the electrical stability of the heart and the development of stress-induced arrhythmia is discussed.

Adaptation, Physiological↗
PubMed1986

[Prevention of heart damage by extreme physical stress and increasing its resistance to acute overstrain with the antioxidant ionol].

A study of the effect of extreme physical stress on the contractility of an isolated heart, its CPK loss associated with anoxia and reoxygenation, and myocardial adenyl components and lactate levels under acute overstrain of the heart achieved through a complete obstruction of the aorta, showed the animals doing exercise to have reduced cardiac contractility, increased perfusate CPK waste, and sharply decreased myocardial macroergic phosphate levels under acute overstrain by pressure. Pretreatment with ionol largely prevented these changes.

Adenine Nucleotides↗
PubMed1986

[Prevention of ischemic and re-oxygenation arrhythmias and heart fibrillation using the antioxidant ionol].

The effect of a synthetic antioxidant, ionol (2,4-ditrebutyl-4-methylphenol) on cardiac arrhythmias induced by 10-minute occlusion of the left coronary artery followed by 5 minutes of reperfusion (RP) was investigated. The study was performed on male Wistar rats, 250-300 g body weight. The animals were ventilated with room air under urethan anesthesia. RP induced more severe ventricular arrhythmias than ischemia (IS). During RP ventricular fibrillation developed in 12 and during IS in 2 out of 24 animals. Other types of arrhythmias--tachycardia and extrasystole--were also more pronounced during RP than during IS. Preadministration of animals with ionol (60 mg/kg, per os) abolished completely ventricular fibrillation during IS and RP. Ionol reduced considerably the incidence of tachycardia and extrasystole, shortening their duration 5-7-fold. The data suggest that the activation of lipid peroxidation may play an important role in the pathogenesis of cardiac fibrillation and open prospects for the prevention and treatment of cardiac arrhythmias with antioxidants.

Animals↗
PubMed1986

[Selective pacemaker interruption and disorders of atrial automaticity during induction of lipid peroxidation].

The influence of lipid peroxidation (LPO) inductor H2O2 on spontaneous contractility and electrical activity of the right atrium was studied. LPO induction caused positive inotropic catecholamine-like effect, followed by brady-arrhythmia with the action of potential prolongation, blockade of electrical activity and atrial arrest. Electrical pacing during atrial arrest caused regular contractions of the same force as before electrical activity blockade. The results suggest that the arrest of spontaneous atrial activity under the influence of LPO inductor is due to the impairment of sinus node automaticity.

Action Potentials↗
PubMed1986

[Prevention of a disorder in the electrical stability of the heart in experimental myocardial infarct by using preliminary adaptation to brief stress exposures and the antioxidant ionol].

Preliminary adaptation to short-term stress was shown to prevent the fall of the heart fibrillation threshold and its increased ectopic activity which is usually observed in experimental myocardial infarction. This protective effect involves an enhanced activity of the organism's antioxidant systems. On this basis, synthetic antioxidant ionol was applied to prevent disturbances of heart electric stability in infarction. Ionol completely prevented the decrease in the electric threshold and the increase in ectopic activity of the heart in experimental infarction, demonstrating thereby an anti-arrhythmic effect.

Adaptation, Physiological↗
PubMed1986

[Effect of vitamin E deficiency on the development of cardiac arrhythmias as affected by acute ischemia].

Malonic dialdehyde content was increased by 53% in the myocardium of male Wistar rats (250-300 g) devoid of vitamin E for 2 months, as compared to the control rats (animals receiving an optimal amount of vitamin E). Transitory ischemia (10 min) with subsequent reoxygenation (5 min) was induced during open heart surgery under urethan anesthesia. Ischemia was induced by the occlusion of the descending branch of the left coronary artery. In ischemic rats with vitamin E deficiency the incidence of ventricular fibrillation, tachycardia, extrasystoles and the additive duration of arrhythmias were significantly increased as compared to the control.

Animals↗
PubMed1986

[Elimination of disorders of electric stability of the heart during post-infarct cardiosclerosis using adaptation to short-term stress and the antioxidant ionol].

The experiments were carried out on male Wistar rats (300-400 g) subject to open chest surgery under nembutal anesthesia. One group of rats with postinfarction cardiosclerosis (PC) was exposed to short-term immobilization stress for 15 days one month after the occlusion of the descending branch of the left coronary artery. The other group of rats with PC was administered synthetic antioxidant ionol (BHT) (60 mg/kg, per os) 3 days prior to the experiments. The electrical stability of the heart was evaluated by assessing ventricular fibrillation threshold (VFT) determined by stimulation of the right ventricular apex by single premature impulses (10 ms) and by measuring the amount of ectopic beats developing during 30-sec stimulation of the right vagus (2 mA, 20 Hz). VFT in rats with PC was significantly lower, as compared to sham-operated rats (2.9 +/- 0.2 and 6.4 +/- 0.2 mA, respectively), with pronounced extrasystoles appearing during vagal bradycardia. In stress-adapted animals with PC VFT returned to the level of sham-operated rats and the amount of premature beats decreased 3-4-fold, as compared to unadapted rats with PC. Ionol (BHT) was shown to have the same effect.

Adaptation, Physiological↗
PubMed1985

Disturbances of the heart structure and function in chronic hemolytic anemia, their compensation with increased coronary flow, and their prevention with ionol, an inhibitor of lipid peroxidation.

The structure and function of heart muscle were studied in rats with chronic hemolytic anemia induced by phenylhydrazine. Contractural lesions, myocytolysis, fatty dystrophy, and small-focal necrosis were found in the myocardium along with hypertrophy. The disturbances were accompanied by a compensatory increase in the coronary flow by 2.5-fold during myocardial contractions. When the coronary flow of isolated hearts was experimentally decreased to the control level, a great depression of the contractile function developed. Administration of the antioxidant ionol, an inhibitor of lipid peroxidation, simultaneously with phenylhydrazine did not prevent the development of the hemolytic anemia, but decreased by 2 times the degree of hypertrophy and the amount of the lesion foci in the heart muscle. It also significantly inhibited the compensatory increase of coronary flow and completely eliminated depression of the heart contractile function during the normalization of coronary flow. The data allow a suggestion that hemolytic anemia is accompanied by activated lipid peroxidation, this process playing a role in the myocardial damage of anemia. Antioxidants can prevent such damage.

Anemia, Hemolytic↗
PubMed1985

[Prevention of disorders in the contractile function of non-ischemic sections of the heart during experimental infarction using beta-endorphin].

The effect of pretreatment with beta-endorphin on disorders of right-atrial myocardial distensibility and contractility in left-ventricular infarction (by Selye) was examined in Wistar rats. This peptide, administered intravenously (50 micrograms/kg) immediately before the simulation of infarction, was shown to reduce considerably infarction-induced impairment of distensibility and contractility of an isolated right atrium and of its resistance to hypoxia and excessive calcium, and also to increase the survival rate. The results of the study suggest that the protective effect of beta-endorphin is chiefly due to its central action.

Animals↗