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Biomedical subjects

F Z Meerson

Publications and source records attributed to F Z Meerson.

At least 127 records · Page 7Linked to original sources
PubMed1989

Adaptation to stress increases the heart resistance to ischemic and reperfusion arrhythmias.

Adaptation to repeated stress prevents or limits ischemic and reperfusion arrhythmias in the whole organism. In studying mechanism of this phenomenon, we have investigated the effect of local ischemia and subsequent reperfusion on the function of isolated hearts of rats adapted to the stress of repeated immobilization. We established that such adaptation limited the depression of the amplitude and velocity of contraction and velocity of relaxation of the heart in ischemia and subsequent reperfusion. Simultaneously this adaptation limited reperfusion-induced arrhythmias to a considerable extent; in particular, the duration of reperfusion-induced fibrillation was reduced two-fold. Thus the cardioprotective antiarrhythmic effect of adaptation of the organism to stress exposure depends not only on adaptive alterations of central regulation, but to a considerable extent, is determined by processes occurring at the level of the heart itself.

Adaptation, Physiological↗
PubMed1989

[Elimination of disorders in the electrical stability of the heart during postinfarct cardiosclerosis by using a factor that induces GABA accumulation in the brain].

It was shown that disturbances of the heart electrical stability in postinfarction cardiosclerosis manifested in a fall of the electrical threshold of the heart fibrillation and the development of extrasystoles during the vagus stimulation. These disturbances were effectively eliminated by administration of GABA in the brain.

Animals↗
PubMed1989

[Antioxidant ionol suppresses ACTH-dependent secretion of corticosterone].

It has been shown that the preliminary administration of a synthetic antioxidant ionol (dibunol, BHT) prevented to a considerable extent the increase in the concentration of corticosterone in the adrenal glands and blood plasma induced by ACTH administration or emotional-painful stress.

Adrenal Glands↗
PubMed1989

[Adaptation to stress increases the resistance of isolated heart to damaging effects of Ca2+ due to optimization of Ca pump function in the sarcoplasmic reticulum].

The adaptation of rats to repeated short-term immobilization stress prevents the calcium-induced arrhythmias and contracture on isolated heart. Obtained results indicate, that main role in this effect plays an increase of both Ca-transport efficiency in sarcoplasmic reticulum and its resistance to autolytic processes.

Adaptation, Physiological↗
PubMed1989

Prevention of cardiac arrhythmias by adaptation to hypoxia: regulatory mechanisms and cardiotropic effect.

Adaptation to intermittent hypoxia had a pronounced antiarrhythmic effect in acute myocardial ischemia in conscious animals. This effect was less pronounced in anesthesia and was absent in isolated heart. In reperfusion, the prophylactic effect of adaptation was equally pronounced in all cases. Adaptation prevented stress-induced exhaustion of brain beta-endorphine presumably by its accumulation in adrenal glands and resulted in the accumulation of dopamine, 5-hydroxytryptamine and 5-hydroxyindolacetic acid in brain structures. These data naturally lead to the assumption that central mechanisms play the main role in the antiarrhythmic effect of adaptation to intermittent hypoxia on ischemic arrhythmias, while mechanisms occurring at the level of heart play the main role in the protective effect of the same adaptation against reperfusion arrhythmias.

Acclimatization↗
PubMed1989

[Elimination of disorders of the electrical stability of the heart in experimental myocardial infarct and postinfarct cardiosclerosis under the influence of a benzodiazepine receptor agonist].

It was shown on Wistar male rats that agonist of benzodiazepine receptors phenazepam considerably suppressed the heart ectopic activity and eliminated disturbances of the heart electric stability in acute myocardial infarction and postinfarction cardiosclerosis. The drug prevented to a considerable extent the death rate of animals within the first day following the ligation of coronary artery and the fall of arterial pressure in animals with the acute myocardial infarction. Possible mechanism of the benzodiazepine agonist effect is under discussion.

Animals↗
PubMed1989

[Prevention of arrhythmogenic and contractile effects of excessive Ca2+ on the heart through adaptation to stress by increasing the activity of sarcoplasmic reticulum].

The experiments with rat isolated hearts and papillary muscles showed that adaptation to short-term stresses increased myocardial resistance to arrhythmogenic and contractile effects of excessive Ca2+. Adaptation caused a three- and fivefold reduction in the contracture and premature beats, respectively, while Ca2+ levels were increased from 1.36 to 10 mM. In the experiments with papillary muscles, the adaptation showed a 6.5-fold decrease in the contracture and significantly limited resting potential depression resulted from lower Na+ concentrations (up to 9 mM) in the perfusion solution. The adaptation to stresses was found to restrict depression of cardiomyocyte electrophysiological parameters that was due to high Ca2+ levels and high heart rate. With the factors, the resting potential in adaptation proved to be significantly higher than in controls and the time of action potential was twice as such as in controls. Biochemical studies demonstrated that Ca2+ transport rates in the sarcoplasmic reticulum, cardiomyocytes of adapted animals were increased by more than 30% whereas the sarcoplasmic reticulum of the heart was more resistant to the effects of endogenous factors of degradation. The authors also discuss a possible mechanism of the cardioprotective effects of adaptation to stress undamaging exposures, which is associated with limited depression of electrophysiological parameters on pathological exposures and with increased Ca2+-transporting capacity of the sarcoplasmic reticulum.

Adaptation, Physiological↗
PubMed1989

[The effect of experimental infarct and emotional-pain stress on the endothelium-dependent reactions of the isolated rat aorta].

Emotional-nociceptive stress, stress induced with a myocardial infarction, and stress following sham operation increased the effect of endothelium on the force and velocity of the smooth muscle contraction. Within 2 hrs after stress and 3 hrs after the coronary artery ligation, a considerable drop occurred in the rat arterial pressure followed by a facilitation of the aorta endothelium-dependent relaxation. Both these parameters were restored to the control level within 24 hrs. The facilitation of the endothelium-dependent relaxation of vascular wall seems to play a role in the drop of the vessels tone, in decrease of arterial pressure and, finally, in development of the cardiogenic shock in myocardial infarction in humans.

Acetylcholine↗
PubMed1989

[Influence of adaptation to stressor effects on bioelectrical activity, contractile function and resistance of the papillary muscles to the excess of intracellular calcium].

In experiments on papillary muscles of rats it was established that adaptation to stressor effects increases resistance of the myocardium to contracture effects and restricts depression of electrophysiological parameters caused by the excess of calcium. Such adaptation decreased contracture by 6.5 times. On the next stage it was established that adaptation restricts depression of electrophysiological parameters of cardiomyocytes with the action of large concentrations of calcium. Possible mechanism of cardiac protector effect of adaptation to stressor effects is being discussed.

Adaptation, Physiological↗
PubMed1989

[The electron microscopic characteristics of stress lung].

The influence of long-term (6 hours) immobilization stress on morphofunctional state of lung air-blood barrier was studied in experiments of the rats. It was shown that stress provoked the marked ultrastructural changes in the lungs, which were as follows: lung tissue oedema, pronounced thickening of lung air-blood barrier and its separate layers, edema-hemorrhagic syndrome, alveolar epithelial injury, disturbance of lung surfactant systems. Such a pathological complex may be designated as a "stress lung".

Animals↗
PubMed1989

[Effect of the antioxidant ionol on energy metabolic indices and heart function during acute hypoxia and subsequent reoxygenation].

The effect of preliminary administration of antioxidant ionol on the heart energy metabolism and contractile function was estimated in hypoxic hypoxia and subsequent reoxygenation. The protective effect of ionol on the energy metabolism in hypoxia was shown to occur mainly at the level of glycolysis. In reoxygenation, the protective effect of ionol manifested at the level of creatine kinase system to provide a rapid restoration of the CP synthesis rate. This shift correlated with the velocity of restoration of the developed pressure and the velocities of contraction and relaxation. On the whole the data obtained correspond to the notion that creatine kinase system and ATP play an important role in the depression and subsequent restoration on the heart contractile function in acute hypoxia and reoxygenation and ionol provides more effective performance of this system and correspondingly more rapid restoration of the contractile function in reoxygenation.

Acute Disease↗
PubMed1989

[Correlations between the endothelium-dependent relaxation of the aorta and arterial pressure in rats with myocardial infarction].

The effect of experimental myocardial infarction on endothelium-dependent relaxation was studied on isolated rat aorta and compared with the dynamics of arterial pressure (AP). It was shown that the endothelium-dependent relaxation of aorta was increased 1.8 times 3 h following the myocardial infarction. Simultaneously the drop in AP which had begun immediately following the experimental infarction became maximal. In 24 h both the indices were restored practically to the initial level. There was a significant negative correlation between the extent of endothelium-dependent relaxation and AP. It was suggested that the increase in endothelium-dependent relaxation could influence vascular tone, the drop in AP, and, finally, the development of cardiogenic shock in myocardial infarction in man.

Animals↗
PubMed1989

[Prevention of adrenaline-induced arrhythmia by a calmodulin blocker, trifluoroperazine].

Adrenergic arrhythmias were induced in isolated rat hearts with epinephrine in a concentration of 5.10(-5) M in the perfusing solution. The rhythm disturbance was accompanied by a pronounced depression of contractility. It was found that the preliminary administration of the calmodulin blocker trifluoperazine (10(-6) M) decreased the duration of arrhythmias and the latency of their development, the contractility remaining at a higher level than in control. Verapamil administered into the perfusing solution did not significantly affect the latency of arrhythmias and reduced the duration of arrhythmias and the cardiotonic effect of epinephrine to a lesser extent than trifluoperazine. The mechanism is under discussion, by which the calmodulin blocker has a more pronounced cardioprotective antiarrhythmic effect than the Ca-channel blocker.

Animals↗
PubMed1989

[Limitation of ischemic necrosis by the use of antioxidant ionol].

Inhibitory effect of Ionol on lipid peroxidation (LPO) in the infarction zone and out of it after experimental myocardial infarction in the experiments on rats was investigated. The results of measurements, performed by two independent methods: point counting and the computer image analysis were compared. It was shown that LPO activation out of the ischaemic zone was prevented and dimensions of the ischaemic necrosis were limited by Ionol, which did not influence LPO activation in the ischaemic zone. Data obtained by both methods coincide qualitatively, the computer image analysis being more sensitive and effective.

Administration, Oral↗