[Adaptation of the body to stress and to altitude hypoxia leads to accumulation of various isoforms of hsp 70 in the myocardium].
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Adaptation, Physiological↗
Biomedical subjects
F Z Meerson
Publications and source records attributed to F Z Meerson.
[Comparative assessment of the effect of adaptation to stress exposure and high altitude hypoxia on heart resistance to reperfusion injury after total ischemia].
Experiments on isolated Wistar rat hearts perfused according to Langendorff showed that adaptation to stress exposure limited the depression of contraction amplitude and contracture and possessed an antiarrhythmic effect in reperfusion. Furthermore, adaptation to stress exposure efficiently limited reperfusion damage to sarcolemma. It was shown that adaptation to hypoxia did not result in any increase in the heart resistance to reperfusion damage following total ischemia. Possible mechanisms of differences in the protective effects of adaptation to stress exposure and hypoxia are discussed.
Adaptation, Physiological↗
[Adaptation of the body to stressors prevents the cardiotoxic effect of rifampicin but not polymyxin B].
It was established on isolated rat hearts that adaptation of the organism to stress exposure effectively limits toxic effect of chronic rifampicin administration (7 mg/kg/day for 8 days) and does not affect the depression of contractile function induced by chronic polymyxin B administration (0.12 mg/kg/day for 8 days). Possible mechanism of the effect of organism's adaptation to stress on the resistance of heart to antibiotics is under discussion.
Adaptation, Physiological↗
[First experience in clinical trials of the new domestic drug acediprol used in the treatment of cardiac arrhythmias].
The antiarrhythmic effect of sodium valproate (acidoprol) on the degree of arrhythmic manifestations was examined in 18 patients with neurocirculatory dystonia (NCD) and 19 with coronary heart disease (CHD). A 24-hour ECG monitoring and recording were performed on emotional stress and exercise. The antiarrhythmic effect of the agent was evaluated by the blind method and placebo. The course of its therapy was found to reduce the frequency of ventricular premature contractions in 14 patients with NCD and to substantially limit or eliminate the arrhythmogenic effect of emotional stress and exercise. In CHD, the antiarrhythmic effect of acedoprol was less, it being shown only by 6 patients, but the effect failed to occur during exercise. However, the arrhythmogenic effect of emotional stress in CHD was significantly limited. Thus, the GAMA-ergic, stress-limiting system activator acedoprol has antiarrhythmic activity in cardiac patients, but its activity is drastically pronounced in NCD and less marked in CHD.
Adult↗
[The effect of adaptation to stress exposures and to periodic hypoxia on the cardiomyocyte trigger activity of the papillary muscles in the rat].
Action potential of cardiomyocytes was recorded in experiments on isolated papillary muscle of the rat left ventricle. The effect was estimated of preliminary adaptation to intermittent hypobaric hypoxia or to short-term stress exposure on the incidence and the pronouncement of delayed after depolarization and of trigger activity induced by a high frequency stimulation against the background of isoproterenol (10(-8) M). It was shown that adaptation to hypoxia or to stress reduced the incidence of delayed after depolarization and of trigger activity, adaptation to stress exerting a more pronounced effect. Immobilization stress (6 hours) potentiated the trigger activity, adaptation to stress exerting a more pronounced effect. Immobilization stress (6 hours) potentiated the trigger activity and this potentiation was effectively prevented by either type of adaptation.
Action Potentials↗
[Disordered cardiac electrical stability in beta-adrenergic damage and antioxidant protection].
The electrical threshold of ventricular fibrillation induced by premature single impulses and the ectopic activity and also an abnormal conduction during vagus inhibition of sinus node were estimated 24 hours after the administration of isoproterenol (10 mg/kg, s/c, on time) in rats. In addition the cardiac contractile function of the left ventricle was studied. The study was performed on male Wistar rats, 250-300 body weight, under nembutal anesthesia. Isoproterenol had no effect on the contractile function in the rest and during maximal isometric load, induced by coarctation of ascending aorta. But in the treated animals the threshold of fibrillation fell more than 2-fold and the vagal bradycardia was more 2-fold then in the untreated animals. The AB-block, idioventricular rhythm and extrasystoles appeared during vagal bradycardia in treated animals, while in the untreated ones there were no any disturbances. The preliminary administration of the antioxidant ionol (BMT, 30 mg/kg, per os, in sun oil) prevented the enumerated shifts.
Animals↗
Adaptation to short-term stress prevents post-infarction hyperactivation of the endothelium and decrease in blood pressure in rats.
The aim of the study was to elucidate the possibility of preventing the decrease in blood pressure (BP) and the endothelial hyperactivation that are induced by experimental myocardial infarction in rats. The endothelial hyperactivation manifested itself in potentiated endothelium-dependent relaxation and in attenuated contractile responses to noradrenaline in isolated rat aortas. Furthermore, the postinfarction changes in BP showed a negative correlation with the endothelium-dependent relaxation. Preliminary adaptation of rats to short-term nondamaging stress exposures or pretreatment with the antioxidant, ionol, prevented to a great extent both the postinfarction decrease in BP and the disturbances in endothelium-mediated responses of smooth muscle. Since, according to the literature, infarction-concomitant stress strongly activates free-radical processes which may result in a hyperproduction of endothelium-derived relaxing factor, it is suggested that the increased potency of anti-oxidant systems is the mechanism common to the protective effects both of adaptation and of ionol.
Acetylcholine↗
[Adaptation of the body to the effects of stress increases the resistance of cardiac nuclei to damaging effects of single-chain exogenous DNA].
The effect of adaptation to stress exposure on the resistance of nuclear DNA to damaging effect of one-chain exogenous DNA was investigated by flow cytometric fluorescence method. It was shown that after the administration of one-chain DNA in concentration of 50 micrograms/ml into the nuclei suspension almost half of nuclear DNA was damaged in control. In adaptation this phenomenon was 5.5 times less pronounced. When the one-chain DNA concentration was increased, this protective effect of adaptation remained. The possible mechanism of the DNA-protective effect of adaptation is under consideration.
Adaptation, Physiological↗
[Effects of adaptation to periodic hypoxia on bioelectric activity of cardiomyocytes of isolated heart in ischemia and reperfusion].
Experiments on isolated Wistar rat heart perfused according to Langendorff showed that preliminary adaptation of rats to intermittent hypobaric hypoxia limited the fall of values of the resting potential and the amplitude and duration of action potential characteristic for ischemia. Under similar conditions, adaptation considerably reduced the increased time of impulse conduction along the myocardium. In reperfusion, the parameters enumerated restored much more efficiently in hearts from adapted animals than in controls. The role of these changes in the antiarrhythmic effect of adaptation to intermittent hypoxia is under discussion.
Action Potentials↗
[Differences in the development of the phenomenon of the adaptive stabilization of the DNA in myocardial nuclei during adaptation to stress and altitude hypoxia: the role of heat shock proteins].
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Adaptation, Physiological↗
[Adaptation to periodic hypoxia limits the demand for ethyl alcohol and the withdrawal syndrome in the chronic alcoholic intoxication of animals].
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Adaptation, Physiological↗
[Formation and reversal development of the local mechanisms of heart protection during adaptation to continuous stress].
Experiments with isolated rat hearts demonstrated that in the course of adaptation to continuous immobilized stress of moderate intensity (1, 5, and 15 days), the heart gradually (at day 15) formed the defense mechanism previously described, that is the adaptive structural stabilization phenomenon (ASSP). ASSP defends cardiac contractile function and has a powerful antiarrhythmic and cytoprotective effect in total ischemia, reperfusion, and under the action of toxic concentrations of calcium and catecholamines. The protective ASSP effect formed over 15 days of continuous stress proved to be steady-state, remaining for 15 days of adaptation cessation. Thus, during adaptation to continuous stress higher regulatory mechanisms determine the gradual development of a highly effective defense mechanism in the heart at the cellular level.
Adaptation, Physiological↗
[Cardioprotective effect of combined use of coenzyme Q9 and cyclohexyladenosine in ischemia, reperfusion and acute myocardial infarction].
Effects of coenzyme Q9 (25 mg/kg), N6-cyclohexyl adenosine (CHA, 100 micrograms/kg) and their combination were compared in rats with short-term or permanent ligation of the left coronary artery. The following parameters were evaluated in three series of experiments: 1) incidence and duration of ventricular fibrillation and tachycardia during coronary occlusion (10 min) and consecutive reperfusion (5 min); 2) contractility and electrical stability of the heart (ventricular fibrillation threshold) in animals with 2-day myocardial infarction; 3) ischemic myocardial mass after coronary occlusion (5 min) and necrotic tissue mass in 2-day myocardial infarction. The rats were given oral drugs 5 days and 2 hours before the study. All the experiments were performed in open-chest anesthetized (nembutal, 50 mg/kg) rats exposed to ventilation at room air. Both the coenzyme Q9 and CHA significantly reduced the incidence and duration of coronary occlusion and reperfusion arrhythmias, prevented cardiac contractile depression (heart rate.developed pressure) and increased ventricular fibrillation threshold). The effect of coenzyme Q9 was more marked than that of CHA. Coenzyme Q9 substantially reduced necrotic tissue mass while CHA diminished ischemic tissue mass. At the same time the total cardioprotective action of the Q9 + CHA combination was more pronounced than that of them used alone.
Adenosine↗
[Correction of disorders of electric stability of the heart and arrhythmia by using a synthetic analog of acetylcholine].
It was shown in experiments on Wistar male rats that ethyl, 3/2, ethyl, 2/2, dimethylhydrazine propionate iodate (EDIHYP), a synthetic acetylcholine analogue, eliminates in situ the fall of the ventricular fibrillation threshold and the extrasystole observed on the background of vagal bradycardia in experimental myocardial infarction and postinfarction cardiosclerosis. The elimination of disturbed heart electric stability was not accompanied by cholinergic, negative chronotropic effect of the drug. In isolated heart, high concentrations of EDIHYP (10(-4) M) had negative chronotropic effect but lacked antiarrhythmic effect in local ischemia and reperfusion. The bradycardia induced by EDIHYP was absent and the antiarrhythmic effect was strikingly pronounced on the background of muscarinic receptors blockade with atropine. Thus EDIHYP realizes its antiarrhythmic effect not via muscarinic receptors but by some other way which requires studying by methods of molecular pharmacology.
Animals↗
[Effects of stress and exercise tests on the functional state of cardiac performance and the state of adrenergic regulation in patients with ischemic heart disease].
In patients with coronary heart disease, stress was found to provoke both ischemic and arrhythmic responses. As compared with exercise test, stress caused arrhythmic reactions more frequently than ischemic ones. Stress was ascertained to provoke ischemic and arrhythmic reactions mainly via increased cardiac function. It also affected the myocardium and coronary bed by the direct action of catecholamines and other stress hormones.
Adolescent↗
[Comparative evaluation of the anti-arrhythmia effect of the antioxidant ionol (dibunol) in the arrhythmic form of neurocirculatory asthenia and stable exertion-induced stenocardia].
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Adolescent↗
[Effect of adaptation to periodic hypoxia on bioelectric activity of cardiomyocytes and cardiac resistance to contractive and arrhythmogenic effects of excessive calcium].
The experiments with isolated hearts from the rats adaptive to a periodic exposure to hypoxia in the barochamber revealed a significant decrease in the contractile and arrhythmogenic effects of high Ca2+ concentrations. With low sodium solution, the contracture and the resting potential depression of cardiomyocytes in the cardiac papillary muscles turned to be less pronounced during adaptation. Increasing the concentration of Ca2+ in the washing solution resulted in lower resting potential, amplitude and duration of the action potential; hypoxic adaptation prevented the changes to a great extent. Whether the changes found may contribute to the anti-arrhythmic effect of periodic hypoxic adaptation is discussed in the paper.
Action Potentials↗
[The role of changes in the bioelectrical activity of the cardiomyocytes in the antiarrhythmic effect of adaptation to hypobaric hypoxia].
The adaptation to periodic hypoxia increases the AP duration in the cardiomyocytes of the rat isolated cardiac papillary muscles; prevents the depression of the resting potential, of the AP amplitude and duration in high calcium concentration and high-frequency stimulation. The adaptation also limits the contracture of papillary muscles and the depression of the resting potential in the cardiomyocytes in hypo-sodium solution. The adaptation seems to enhance the efficacy of the membrane mechanisms of the ion transport in cardiomyocytes, whereas subsequent changes in bioelectrical activity play a major part in antiarrhythmic effect of the adaptation.
Action Potentials↗