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Biomedical subjects

F Z Meerson

Publications and source records attributed to F Z Meerson.

At least 109 records · Page 6Linked to original sources
PubMed1990

[Comparative evaluation of anticonvulsant and anti-arrhythmic effects of phenazepam, a benzodiazepine receptor agonist].

It was established on white mice that benzodiazepine receptor agonist phenazepam possessed a high anticonvulsant activity to antagonize bicuculline, corrasol, picrotoxin and thiosemicarbazide. It was also shown that phenazepam had a potent antiarrhythmic effect on ischemic and reperfusion cardiac arrhythmias in Wistar rats in situ. The effect was of a central nature since it was irreproducible in isolated heart. It seems to be due to the potentiating effect of phenazepam on the realization of GABA inhibitory control of centers of the heart regulation. The facts obtained evidence a possibility of using phenazepam not only as an anticonvulsant but also as an antiarrhythmic means.

Animals↗
PubMed1990

[Relations of catecholamine and prostaglandin contents in the blood of rats exposed to acute stress and during adaptation to stress].

In Wistar male rats, 1-h acute immobilization stress resulted in the increased plasma adrenalin, noradrenaline and dopamine in approximately 13, 8 and 23 times, respectively. Plasma PGF2 alpha increased in 3.5 times while PGE remained unchanged; this resulted in the decreased PGE/PGF2 alpha relation in 2.8 times. The PGI2/TXA2 relation also decreased in 1.5 times due to a more pronounced growth of TXA2 than that of PGI2. In rats adapted to the repeated stress (12 sessions), the plasma catecholamine level was higher than that in control but 2-3 fold lower than in unadapted rats after acute single stress. In this situation, PGE was increased by 70% as compared to the control. This is why PGE/PGF2 alpha relation was similar to the control whereas the level of PGF2 alpha increased. PGI2 increased by 53% and TXA2--in two times as compared to the control. In these rats, acute stress induced neither plasma catecholamine enhancement nor PGE/PGF2 alpha relation decrease in comparison with the initial levels; the TXA2 content was increased but it was by 33% less than that in unadapted rats exposed to such stress. One can suggest that the decreased activation of adrenergic system respondent to acute stress in unadapted rats is associated with the increase in plasma PGE and PGI2 which are known to limit the catecholamine release from adrenergic terminals and their harmful effects.

Acute Disease↗
PubMed1990

Increased resistance of the cardiac sarcoplasmic reticulum Ca(2+)-pump to autolysis after adaptation of rats to stress.

Experiments on rats are reported in which Ca2+ uptake by the sarcoplasmic reticulum (SR) and the time course of SR Ca(2+)-pump inactivation and Ca2+ leakage from intracellular compartments into the incubation medium were studied in tissue homogenates stored at 4 degrees C. Long-term (6 h) immobilization stress significantly reduced the ability of the SR to take up Ca2+, accelerating (two- to threefold) both Ca(2+)-pump inactivation and Ca2+ leakage induced by autolysis during storage. A course of adaptation to repeated short-term stress prevented the adverse effects of long-term stress on the SR Ca(2+)-pump. Adaptation to repeated stress itself accelerated the rate of Ca2+ uptake by the SR and sharply inhibited the SR Ca(2+)-pump inactivation and Ca2+ leakage induced by autolysis. Possible mechanisms for the adaptive stabilization of SR membranes against factors that cause autolysis are discussed.

Adaptation, Physiological↗
PubMed1990

[Anti-arrhythmic effect of adaptative activation of the vagus nerve system and a new synthetic acetylcholine analog].

A higher vagal tone or its stimulation under certain conditions is known to increase the threshold of cardiac fibrillation and even to arrest developing arrhythmias. This effect is usually evaluated as a result of limiting the excessive adrenergic effect on the heart, which is observed in stress and ischemia. The following two facts have been first identified: 1) adaptation to moderate continuous stress may induce tonic excitation of parasympathetic regulation of the heart and enhance its resistance to ischemic and reperfusion arrhythmias; 2) this antiarrhythmic effect is completely reproducible by the recently synthesized acetylcholine analogue EDIHYP, ethyl-3/2-ethyl-2,2-dimethylhydrazinium/propionate iodate.

Acetylcholine↗
PubMed1990

[Effects of adaptation to exposure to short-term stress on indices of resistance of energy metabolism and contractile function of the myocardium to acute hypoxic hypoxia and reoxygenation].

Effect of preliminary adaptation to immobilization stress with progressive duration from 15 min. to 1 h (every second day, 8 sessions) on the resistance of indices of myocardial energy metabolism and contractile function to acute hypoxic hypoxia and subsequent reoxygenation was studied. It was shown, that adaptation to short-term stress exposure by some way provided the retention of activities of important enzymes like creatine-phosphokinase and phosphorylase under the harmful action of acute hypoxia and subsequent reoxygenation. At the same time, the ATP restoration and the CP super-restoration were observed during reoxygenation. This effect, in its turn, was accompanied by a more pronounced super-restoration of the heart contractile function than in control.

Acute Disease↗
PubMed1990

[Disorders of supporting mechanisms of resting membrane potentials of the cardiomyocytes during stress and their prevention].

Incubation of the rats' hearts in low temperature (4 degrees C) in the course of 1.5 h reduced the rest membrane potential (RP) of the cardiomyocytes from 86 +/- 2 to 60 +/- 2 mv. Rapid rewarming to 36 degrees C resulted in hyperpolarization of the membrane potential to 103 +/- 3 mv with maximal speed of restitution of RP about 0.35 mv/sec. These results were determined by electrogenic Na-pump. In the heart of rats, exposed to 6-hour immobilization stress, the speed of restitution of RP decreased to 0.15 +/- 0.01 mv/sec and the hyperpolarization effect was eliminated. This was indicated on the disturbance of Na-pump of the cardiomyocytes membranes. Preliminary treatment with gamma-hydroxybutyric acid or antioxidants alpha-tocopherol and ionol prevented stress-induced disturbances of the cardiomyocytes.

Animals↗
PubMed1990

[Effects of short and long term immobilization stress on the functioning of Ca pump of the sarcoplasmic reticulum and cardiac resistance to Ca2+ excess].

In the experiments on rats a significant decrease of resistance to the contracture and arrhythmogenic effect of increased Ca2+ on the isolated hearts of animals after short term immobilization stress has been shown. After a long term stress (6 hours) the changes of the studied physiological parameters of the isolated hearts were not observed. Transport in the homogenates of the rat hearts was measured by the Ca--selective electrode on the ionometer ORION EA 940. After a 1-hour stress the rate of Ca--transport in sarcoplasmic reticulum (SR) substantially decreased as compared with the control (3.5 fold at 20 mcM), but at the higher concentration the Ca-transport was inhibited. The long term stress lead to a slower damage of functional Ca-transport system of SR--at 20 mcM the rate decreased by 25% as compared with control and at the higher concentration of Ca2+ depression of transport was not observed.

Animals↗
PubMed1990

[Adaptation to stress exposure prevents the arrhythmogenic and contractile effects of the "calcium paradox"].

It was established in experiment on rat papillary muscle that adaptation to stress exposure increased the myocardial resistance to contractile actions and limited the depression of electrophysiologic parameters induced by the excess of intracellular calcium. This adaptation decreased the contracture in 6.5 times and significantly limited the depression of resting potential (RP) induced by low-sodium (9 mM) perfusing solution. It was shown at the next stage that adaptation limited the depression of electrophysiologic parameters of cardiac cells at high calcium concentrations and high pacing rate. Under these factors the resting potential appeared to be significantly more in adaptation than in control (82 mV vs 69 mV respectively) while the action potential (AP) duration was twofold more. Possible mechanism is discussed of the cardioprotective effect of adaptation to stress exposure associated with the limitation of RP and AP in calcium overload.

Adaptation, Physiological↗
PubMed1990

[Increased vagal tone in adaptation to the effects of continuous stress and termination of cardiac arrhythmias].

It was established in experiments on rats exposed to 5 day stress that 1 day stress resulted in a twofold decreased heart fibrillation threshold (HFT) and 5 day stress resulted in bradycardia and in the restoration of HFT to the control level. The restoration of the heart electric stability was due to an increased vagal tone because atropine eliminated the bradycardia and reduced HFT again. Adaptation to continuous 5 day stress increased 3-7-fold the heart resistance to ischemic and reperfusion arrhythmias. This protective effect was completely abolished with atropine. Thus adaptation to continuous mild stress has a potent antiarrhythmic effect which occurs due to the increased vagal tone.

Adaptation, Physiological↗
PubMed1990

[Phenomenon of adaptive stabilization of cardiac structures and their protection].

Animal adaptation to repeated non-damaging stresses was shown to lead to the development of a phenomenon of adaptive stabilization of cardiac cellular structures. In isolated hearts, it appeared as a multifold decrease in reperfusion-induced arrhythmia severity, a sharply limited release of enzymes during the reperfusion paradox, and a lack or reduction in the contracture due to high calcium concentrations. The sarcoplasmic reticulum and mitochondria isolated from these hearts were found to be much more resistant to autolysis than the controls and to retain their function during prolonged storage. After coronary ligation in the adapted animals, the zone of acute ischemia was identical to that in the controls, and the necrotic zone measured 2 days later was reduced by more than 40%. Thus, the phenomenon of adaptive stabilization of cellular structures possesses no anti-ischemic effect, but forms the basis for a strong cytoprotective effect, thus providing protection of the heart from the necrotic action of ischemia. The author also discusses whether the genetic mechanism may be responsible for the phenomenon of adaptive stabilization of the structures and stress proteins may make a contribution to the phenomenon.

Adaptation, Physiological↗
PubMed1990

[Effect of stress of "struggle" and the stress of "capitulation" on the resistance of the myocardium to excessive level of calcium].

The resistance of isolated, perfused by Langendorf the heart was compared in the experiments on Wistar rats with elevated by 7.3 times the concentration of the calcium in perfused solution. It was shown that one-hour stress of the "struggle" raised but six-hour one decreased the resistance of the heart to arrhythmogenic and contraction action of the surplus Ca2+.

Animals↗
PubMed1990

[Effects of stress and exercise on rhythm activity of the heart and state of adrenergic regulation in patients with neurocirculatory dystonia].

Responses of healthy subjects and patients with a cardiac type neurocirculatory dystonia (NCD) to exercise and stress were evaluated. Stress was ascertained to cause a higher enhancement of catecholamine excretion than exercise. In patients with NCD, resting adrenaline (A) excretion was increased by 50%, whereas the noradrenaline (NA) one remained unchanged. The A/NA ratio showed a more than 1.5-fold increase. A stress-induced rise in NA excretion was 4 times higher in NCD patients than in healthy subjects. In the patients, resting dopamine (D) excretion was lower and the D/A + NA ratio was decreased both at rest and during exercise. In NCD the higher adrenergic response to stress was followed by the occurrence of arrhythmias in more than a half of the patients. The healthy subjects and the patients with NCD developed no arrhythmias during exercise. It has been suggested that changes in adrenergic control and associated arrhythmias are caused by dysfunction of the stress-limiting systems in NCD.

Adolescent↗