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Biomedical subjects

F Z Meerson

Publications and source records attributed to F Z Meerson.

At least 145 records · Page 8Linked to original sources
PubMed1988

[Decreased chemoreactivity of neurons of the sensorimotor cortex during adaptation to stress and its role in the prevention of heart fibrillation in acute ischemia].

The effect of the adaptation to repeated short-term stress on the bioelectrical responses of neurons in the IV layer of the sensorimotor cortex developed under the action of acetylcholine and norepinephrine was studied in rats along with the effects on the development of arrhythmias, fibrillation and mortality in conscious animals with cardiac ischemia. It has been established that the preliminary adaptation reduced considerably the chemoreactivity and especially adrenoreactivity of the neurons and at the same time decreased fibrillation and mortality in acute ischemia.

Acetylcholine↗
PubMed1988

[Prevention of arrhythmia in acute ischemia in conscious animals using a serotonin analog].

The state of the serotonergic system was studied in adaptation of rats to short-term non-damaging stress actions along with the possibility of protecting the heart of conscious animals against arrhythmias in acute ischemia with the serotonin analogue 4-nitro-5-methoxytryptamine. It was shown that the adaptation resulted in a significant increase in rat midbrain serotonin by 70%. Preliminary administration of the serotonin analogue 3 fold reduced the total duration of arrhythmias and approximately 5 fold--the heart fibrillation rate and the death rate of animals in acute ischemia. The data obtained are in agreement with the idea on the role of stress-limiting systems in prevention of stress-induced and ischemic damages of the organism. They show that protective effects of metabolites of these systems can be successfully reproduced with their synthetic analogues or activators.

5-Methoxytryptamine↗
PubMed1988

[Effect of adaptation to hypoxia on the antioxidant enzyme activity in the liver in animals that have undergone stress].

It was shown in experiments on rats that emotional-painful stress resulted in a rapid increase in malonic dialdehyde (MDA) and in a decrease in the activity of superoxide dismutase (SOD) in liver. Adaptation to moderate intermittent hypoxia in altitude chamber did not affect MDA and increased hepatic SOD by 65%. Stress exposure caused no change in SOD and MDA, but abruptly reduced the fall of SOD in adapted animals. These data are in accordance with the well-known idea that adaptation to hypoxia prevents the activation of lipid peroxidation and the hepatic damage in stress.

Adaptation, Physiological↗
PubMed1988

[Selective suppression of lipid peroxidation in the brain under stress].

The time course of lipid peroxidation (LP) products was studied in the heart, liver, and brain of rats exposed to 1, 6 and 12 h stress and compared with the extent of LP induction in these organs in vitro. It was shown that the LP activation in the internal organs with maximum in 1 h stress was accompanied by 2 fold decrease in LP products in the brain. More prolonged stress eliminated differences between tissues in all organs approaching the LP level to the control. The LP induction in vitro also revealed reciprocal relations between the LP intensity in brain and internal organs which remained in control group as well. Possible role of the LP suppression in brain induced by acute stress and significance of the phenomenon are under discussion.

Animals↗
PubMed1988

[Effect of adaptation to stress exposures on the cholino- and adrenoreactivity of the atria and their content of acetylcholine in rats with myocardial infarct].

The effect of left-ventricular myocardial infarction (MI) on cholino- and adrenoreactivity of an isolated right atrium and acetylcholine (AC) content of both atria was evaluated experimentally in Wistar rats, adapted or unadapted (control) to stress. In the control sample, 24-hour-long MI increased the chronotropic response to AC, while atrial endogenic AC dropped fourfold. Those changes were accompanied by no marked changes in pacemaker adrenoreactivity. Adaptation to stress reduced pacemaker choline reactivity without any significant effect on pacemaker adrenoreactivity or atrial AC. At the same time, adaptation largely prevented MI-induced increase in pacemaker choline reactivity and atrial AC drop. Increased pacemaker choline reactivity, seen in MI, enhances pacemaker sensitivity to cognition of ectopic excitation foci and, hence, cholinergic effects, that may promote the emergence of arrhythmia. Therefore, pacemaker resistance to cholinergic action, increasing in the course of adaptation, may be an important element of the protective antiarrhythmic effect of adaptation to stress in MI.

Acetylcholine↗
PubMed1988

[Elimination of stress-induced activation of DNA reparative synthesis in the myocardium by increasing the load on the heart].

The rate of DNA reparative synthesis was studied in the nucleus of myocardial cells in the heart compensatory hyperfunction (HCH) induced by the aorta coarctation and in animals exposed to surgical stress without the aorta coarctation. It was established that both surgery and emotional painful stress activated the DNA reparative synthesis in myocardial cells. For example, 12-24 hrs following the surgery the DNA reparation rate exceeded control values by 50-74%. HCH induced no changes in the DNA reparation rate in nuclei of myocardial cells. The mechanism of stress-induced DNA damage is discussed and a hypothesis is put forward on stabilizing the effect of hyperfunction on the DNA structure.

Animals↗
PubMed1988

[Increased level of immunoreactive opioid peptides in the brain and adrenals of rats as affected by adaptation to physical loading].

The effect of long-term (7 weeks) swimming training on the content of beta-endorphin, met- and leu-enkephalins in various brain regions and adrenal glands has been studied in Wistar rats. It has been shown that the adaptation to exercise induced an increase in the content of opioid peptides in most of the brain regions and in adrenal glands. This increase in the level of opioid peptides seems to play an important role in the increase of the resistance to stress.

Adaptation, Physiological↗
PubMed1988

[Enhanced resistance of the heart to arrhythmogenic factors as affected by adaptation of the body to stress exposures].

Adaptation to short-term nondamaging stress effects largely limits or prevents cardiac arrhythmias in acute ischemia and reperfusion. The study examines to what extent this anti-arrhythmic effect depends on adaptational shifts of the heart itself. Isolated hearts of animals adapted to stress are shown to possess dramatically increased resistance to arrhythmias induced by local ischemia and reperfusion. The role of activated prostaglandin biosynthesis, adenosine, antioxidant systems, desensitization and other protective control systems functioning at heart level to provide this anti-arrhythmic effect is discussed.

Adaptation, Physiological↗
PubMed1988

[Effects of adaptation to periodic and continuous hypoxia in disorders of electrical stability of the heart in postinfarction cardiosclerosis].

The effects of adaptation to intermittent and continuous hypoxia on the electrical stability of the heart were compared in middle altitude conditions and in altitude chamber in Wistar rats with postinfarction cardiosclerosis. It has been shown that both forms of adaptation could restore the heart fibrillation threshold and restrict the ectopic activity in postinfarction cardiosclerosis. Beneficial effects of adaptation to intermittent hypoxia in conditions of the altitude chamber appeared to be more radical.

Adaptation, Physiological↗
PubMed1988

[Prevention of ischemic and reperfusion arrhythmias using the calmodulin blocker trifluoperazine].

Models of ischemic and reperfusion arrhythmias were reproduced in isolated rat hearts by means of the ligation and subsequent reocclusion of the left descending coronary artery. The introduction of trifluoperazine (TFP, 10(-6) M) and verapamil (2.5 X 10(-8) M) into the perfusion medium produced a 20% depression of contractility in aerobic conditions; an additional depression of contractility at 20 min of ischemia and 10 min of reperfusion was 40 and 50%, respectively, for TFP and about the same for verapamil, as compared to the control. Antiarrhythmic effect of TFP was much higher, as compared to that of verapamil. The calmodulin blocker reduced fivefold total duration of arrhythmias, whereas the calcium-incorporation blocker only reduced it by 2.5 times. The antiarrhythmic effect of TFP was even more marked, as compared to verapamil, at reperfusion: TFP reduced total duration of ventricular tachycardias and ventricular fibrillations by 2 and 35 times, respectively, while verapamil had no effect on those types of arrhythmia. A possible mechanism of antiarrhythmic action of the calmodulin blocker TFP is discussed.

Animals↗
PubMed1987

Prevention and elimination of heart arrhythmias by adaptation to intermittent high altitude hypoxia.

It was shown that adaptation to intermittent hypoxia in altitude chamber prevented the poststress fall of the electrical threshold of heart fibrillation. In acute ischemia, the number of fibrillation episodes and the death rate of preadapted animals were 2-3 fold lower than in controls. The adaptation to hypoxia resulted in a significant increase in concentration of opioid peptide beta-endorphin in adrenal glands while stress-induced changes in beta-endorphin in brain structures of adapted animals were much less pronounced. In animals with postinfarction cardiosclerosis, the course of hypoxic actions resulted in restoration of the decreased heart fibrillation threshold, reduced the heart ectopic activity which had developed on the background of vagal bradycardia, and eliminated depression of the heart contractile function. Simultaneously, the adaptation induced a decrease of the postinfarction scar by one-third and an increase of vascularization of the myocardial zone adjacent to the scar.

Adaptation, Physiological↗
PubMed1987

[Prevention of arrhythmias and cardiac fibrillation in acute ischemia and reperfusion by using a factor causing GABA accumulation in the brain].

Anticonvulsant sodium valproate, an inhibitor of GABA transaminase, which induces GABA accumulation in the brain, has been shown to possess a potent antiarrhythmic effect. In acute ischemia and reperfusion in conscious rats with closed chest, it decreased fourfold total duration of arrhythmias, while in nonanesthetized animals with open chest, it substantially limited the heart electrical fibrillation threshold and reduced fourfold total duration of arrhythmias. In both experimental models, sodium valproate decreased threefold the rate of ischemia-induced heart fibrillations. Clinicophysiological evaluation of the effect of sodium valproate on arrhythmias in coronary patients appears warranted.

Acute Disease↗
PubMed1987

[Rehabilitative effect of adaptation to hypoxia in experimental post-infarct cardiosclerosis].

Electrical cardiac fibrillation threshold was shown to be reduced twofold 2 months after the induction of experimental infarction in animals with postinfarction cardiosclerosis. Major contractility parameters at rest and under isometric load on the heart were also reduced essentially in these animals. Gradual postinfarction adaptation to high-altitude hypoxia in an altitude chamber resulted in a considerable (60%) increase in fibrillation threshold and virtually complete recovery of myocardial contractility, as well as a twofold reduction in scarred tissue mass. Possible use of adaptation to hypoxia for postinfarction rehabilitation on in man is discussed.

Adaptation, Physiological↗
PubMed1987

[Effect of preliminary adaptation to moderate and intensive physical loads on cardiac electrical stability and contractile function in experimental myocardial infarct].

Preliminary adaptation of animals to a moderate swimming exercise prevented the fall of ventricular fibrillation electrical threshold and limited drastically the heart ectopic activity in acute myocardial infarction. Adaptation to intense stress, i.e. prolonged swimming with a load, had less preventive effect. The rationing of preventive exercise, to be used for the prophylaxis of myocardial infarction, is discussed.

Adaptation, Physiological↗