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Biomedical subjects

F Z Meerson

Publications and source records attributed to F Z Meerson.

At least 73 records · Page 4Linked to original sources
PubMed1992

[Effects of synthetic antioxidant ionol on bioelectric activity of cardiomyocytes and arrhythmia in global ischemia and reperfusion of the isolated rat heart].

Isolated rat hearts were subjected to global ischemia (15 min) and reperfusion (20 min). Transmembrane potentials were recorded on the epicardial surface and contractile force was measured. Ischemia reduced the resting potential, the action potential (AP) amplitude and the AP duration (APD) in control animals. Pretreatment with synthetic antioxidant ionol (BHT, 50 mg/kg, per os) didn't influence the time course of changes in the resting potential and AP amplitude during ischemia, but significantly increased APD. In the pretreated group, 5 min after the aorta clamping, the APD at 50% and 90% levels of repolarization was 36% (p less than 0.05) and 13% (p less than 0.1) higher in comparison to the preischemic level and 10 min after clamping by 27% (p less than 0.1) and 29% (p less than 0.05), respectively. By the end of ischemia in the pretreated group, APD re-decreased almost to basal level, but in control group, it remained decreased. During reperfusion BHT improved the recovery of bioelectrical activity and the contractile function. The BHT 10-fold reduced the malignant arrhythmias duration and 2.5-fold the incidence of ventricular tachycardia and fibrillation during reperfusion. These results indicate that the induced by BHT increase in APD can contribute to the mechanism of BHT antiarrhythmic action.

Action Potentials↗
PubMed1992

[The role of the prostaglandin system in the cardioprotective effect of adaptation to hypoxia in stress].

The adaptation to periodic altitude hypoxia is known to have cardioprotective and antiarrhythmic effects in stress-induced and ischemic lesions. The effects are assumed to be associated with the enhanced activity of the body's stress-limiting systems, including prostaglandins (PG). Wistar rats were adapted in a hypobaric chamber at an altitude of 4000 m for 6 hours during 40 days. The levels of myocardial and plasma PGE, PGE2 alpha, PGI2, thromboxane A2 were measured by radioimmunoassay and those of plasma catecholamines by enzyme radioassay. In the myocardium, the adaptation showed a 2-fold increase in PGE levels, the PGE/PGE2 alpha ratio and PGI2 levels rose by 70 and 73%, respectively, the PGI2/thromboxane A2 ratio remaining unchanged, while thromboxane A2 concentrations also rose. In adaptation, the levels of PGE and PGI2 was 78 and 60% higher, respectively. In restraint stress, myocardial and plasma PG levels proved to be substantially higher in adapted animals than in the controls, but stress-induced plasma catecholamine release, i.e. stress reaction, showed a 2-3-fold decrease that in the controls undergoing the same stress. The findings along with the data on the cytoprotective and vasodilating action of PGE and PGI2 suggest that enhanced activity of the myocardial and blood PG system is the important link in the mechanism responsible for the antistress impact of adaptation.

Adaptation, Physiological↗
PubMed1992

[Cardioprotective effects of adaptation to restraint stress and hypoxia].

Isolated rat heart experiments have revealed that restraint stress adaptation results in enhanced resistance of the isolated heart to reperfusion. There is also a higher resistance to the autolysis of the organelles isolated from the hearts of stress-adapted animals. This complex of changes is designated as a phenomenon of adaptive stabilization of structures (PhASS). The phenomenon developing in restraint stress adaptation substantially limits arrhythmias, contracture, contraction amplitude depression, and creatine kinase release into the perfusate in thermal damage to the isolated rat heart. Simultaneously, PhASS is accompanied by a multiple increase in five hsp70 isoforms with pI 5.8-6.3 in cytosol and two isoforms with pI about 6.3 in the nucleoplasm. Only two hsp70 isoforms with pI about 5.8 accumulate solely in cytosol during adaptation to intermittent hypoxia. Consistently, the resistance of Ca(2+)-pump and nuclear DNA remains unchanged and the protection against reperfusion and thermal damage are several times less pronounced.

Adaptation, Physiological↗
PubMed1992

[Effects of adaptation to periodic hypoxia on Ca2+ pump of the cardiac sarcoplasmic reticulum and its resistance to endogenous damaging factors].

The adaptation of rats to periodic "altitude" hypoxia in the altitude chamber (6 hour daily at an altitude of 5000 m during a month) led to increased activity of the Ca2+ pump in the myocardial sarcoplasmic reticulum, which was associated with lower Kd values and higher calcium transport Vmax. When a cardiac homogenate was kept at 4 degrees C, autolysis resulted in a decrease in Ca2+ pump activity (which was more rapid in adapted animals than in the controls) and an equal increase in the levels of free calcium in the homogenates in the two series of experiments. The approximate data were obtained when a homogenate was incubated at 37 degrees C, but when it was incubated at 4 degrees C, the rate of Ca(2+)-pump inactivation decreased 20-fold. Incubation in the presence of free radical oxidative inductors (Fe2+ ascorbate) led to high resistance of myocardial Ca(2+)-pump in the adapted rats. The paper discusses the causes of myocardial Ca(2+)-pump activation in periodic hypoxic adaptation and the mechanisms for its increased resistance to active oxygen, as well as their role in the cardioprotective effect of the adaptation.

Adaptation, Physiological↗
PubMed1992

[Opposite effects on antioxidant enzymes of adaptation to continuous and intermittent hypoxia].

Adaptation to continuous hypoxia under mid-mountain conditions (altitude 2100 m) decreases the content of lipid peroxidation products and the activity of superoxide dismutase and catalase in rat heart, liver, and brain, with a concomitant decline in the resistance to reperfusion arrhythmias. On the contrary, adaptation to intermittent hypoxia in the altitude chamber increases the activity of the antioxidant enzymes in the same organs, while the content of peroxidation products remains normal; at the same time, the heart becomes more resistant to reperfusion arrhythmias. The mechanism is discussed that ensures enhanced antioxidant protection in adaptation to intermittent hypoxia.

Adaptation, Physiological↗
PubMed1992

[Isoform pattern of inducible HSP 70 in the rat myocardium after heat shock].

The hsp 70 content was measured in the myocardium of a control rat group, in the group of rats 24 hours following a heat shock and in the group of rats 48 hours after a heat shock. In 24 hours after the heat shock, a major inducible hsp 70 with molecular weight of 71 kDa and pI about 5.8 occurred which was utterly absent in myocardial cytosol from control animals. In addition, there was an increase in polypeptide fraction with molecular weight of 73 kDa and pI about 5.6 (HSX73). In 48 hours after the heat shock, first the inducible hsp 70 with molecular weight of 71 kDa and pI about 5.8 disappeared which was found in 24 hours; secondly, HSX73 decreased to the control level and, thirdly, several isoforms pronouncedly accumulated with molecular weight of about 71 kDa and pI ranging from 5.9 to 6.3. Thus, the isoform composition of stress proteins induced by heat shock strongly depends on the time after the stress exposure. Furthermore, the accumulation of more acidic isoforms precedes the accumulation of alkaline ones.

Animals↗
PubMed1992

Phenomenon of the adaptive stabilization of structures and protection of the heart.

OBJECTIVE: To study the role of heat shock proteins in the mechanism of adaptive stabilization of structures. DESIGN: Double-blind randomized trial. ANIMALS: Wistar male rats weighting between 250 and 300 g. INTERVENTIONS: Adaptation to restraint stress. Animals were heparinized and anesthetized with nembutal. Experiments on isolated heart included ischemia, reperfusion, adrenergic damage and heat shock. Biochemical investigations studied calcium transport from sarcoplasmic reticulum and mitochondria, and cytofluorimetrical analysis of DNA using the O'Farrell method. MAIN RESULTS: In reperfusion, the contraction amplitude of the hearts from adapted animals was 8.8 times higher than control. This acceleration of the contractile function recovery was due to a more rapid disappearance of the contracture. The duration of ventricular tachycardia and fibrillation was 246 +/- 16 s in control and 119 +/- 12 s in adaptation (P < 0.001). The creatine kinase release was 719 +/- 34 mU/min/g wet weight in control and 302 +/- 120 mU/min/g wet weight in adaptation (P < 0.05). In adaptation, the heat shock-induced contraction amplitude was 2.4 times higher than control and the enzyme yield was practically absent. Adaptation reduced the duration of atrioventricular blockade from 385 to 233 s per group and decreased the number of extrasystoles by 6.5 times. The calcium leakage from intracellular stores during storage proceeded slower in adaptation than in control. During storage of mitochondria at 4 degrees C, oxygen consumption fell much slower in adaptation than in control. As a result, the capacity of mitochondria (isolated from hearts of adapted animals stored for two days) to consume oxygen was 50% higher than in controls; in controls, almost one-half of nuclei were already damaged at one-chain DNA concentration of 50 micrograms/mL, while this phenomenon was 5.5 times less pronounced in adaptation. Adaptation resulted in the accumulation of five polypeptides (molecular weight 72 kDa and pl from 6.3 to 5.7). CONCLUSIONS: The mechanism providing adaptive increase of the heart resistance is apparent both at the central level and at the level of heart cells, and is accompanied by accumulation of inducible polypeptides.

Adaptation, Physiological↗
PubMed1991

Phenomenon of the adaptive stabilization of sarcoplasmic and nuclear structures in myocardium.

In adaptation of rats to repeated stress exposure, a mechanism gradually forms at the level of heart to provide a considerable increase in the organ resistance to reperfusion paradox and toxic concentrations of catecholamines and Ca2+. Sarcoplasmic reticulum and mitochondria isolated from the hearts of adapted animals are highly resistant to autolysis, and nuclei to the damaging action of one-chain DNA. These changes are named phenomenon of the adaptive stabilization of structures (PhASS). An important role of myocardial heat shock protein (HSP) accumulation in the mechanism of PhASS is shown. The development of PhASS is accompanied by an increased resistance of myocardium to ischemic necrosis.

Adaptation, Physiological↗
PubMed1991

[Increase of alpha 1-adrenoreactivity of the rat heart in adaptation to periodic hypoxia].

There is a possibility that the cardioprotective effect of adaptation to intermittent hypoxia is due to changes in receptors apparatus of the heart. In this connection the effect of preliminary adaptation to intermittent hypoxia (4 hours per day at the altitude of 4000 m during 40 days) on the state of beta-receptors-adenylate-cyclase system and same other receptors of the heart were studied. It was shown that at the end of the course of adaptation the number of beta-adrenoceptors in the heart was increased with simultaneous decrease in basal adenylate-cyclase activity, accompanied by the diminution of its response to beta-agonist. The number of beta-adrenoceptors was increased by 48% and their affinity to ligand was increased by almost 2 times. The revealed decrease in the reactivity of beta-receptor-adenylate-cyclase system and increase of alpha 1-adrenoreactivity can play a certain role in the mechanism of cardioprotective effect of adaptation to hypoxia.

Adaptation, Physiological↗
PubMed1991

[Adaptation to short stress exposures prevents the enhancement of the endothelium-dependent reactions of the aorta in myocardial infarct].

Acute stress concomitant to the experimental myocardial infarction resulted in endothelial hyperactivation in the rat aorta as manifested in an increased inhibition of norepinephrine-induced contractions of smooth muscle, enhanced endothelium-dependent relaxation and a respective drop of the blood pressure. Preliminary adaptation of rats to short-term non-damaging stress exposure to a considerable extent prevented the stress-induced hyperactivation of endothelium and improved the postinfarction time course of the blood pressure.

Adaptation, Physiological↗
PubMed1991

[The prevention of a postinfarct fall in pressure and hyperactivation of the aortic endothelium in the rat by using the antioxidant ionol].

The stress concomitant with experimental myocardial infarction resulted in endothelial hyperactivation of the isolated rat aorta. The hyperactivation was manifested in potentiated inhibition of norepinephrine-induced contractions of vascular smooth muscle, increased endothelium-dependent relaxation and respective drop of systemic blood pressure. Preliminary treatment of animals with synthetic antioxidant ionol prevented the stress-induced endothelial hyperactivation and beneficially affected the postinfarction time course of blood pressure. The data suggest that the endothelial hyperactivation observed in acute myocardial infarction is induced by stress-induced activation of free-radical oxidation which results in a hyperproduction of endothelium-derived relaxing factor (nitric oxide).

Animals↗
PubMed1991

[The role of occupational and social stress in the development of non-ischemic arrhythmia in pilots].

In the absence of coronary heart disease and ischemic responses to exercise, many highly skilled pilots have been shown to have arrhythmias of non-ischemic origin. The occupational stress-exercise on a flight trainer reveals such arrhythmias much more frequently than bicycle ergometric exercise. Under social stress, namely during medical- and flying examination which decides if a pilot is professionally fit, 24-hour monitoring in the out- and inpatient settings detects premature+ ventricular contractions of non-ischemic origin in high-grade pilots; the contractions regularly decreasing or ceasing during a true flight. Thus, the social stress in pilots is a stronger arrhythmogenic factor than is the routine occupational stress.

Adult↗
PubMed1991

[Adaptive stabilization of myocardium under the influence of electroacupuncture and cardiac protection].

Adaptation of animals to short-term stress is known to result in the development of the adaptive structure stabilization phenomenon. At the level of the heart, the phenomenon appears as increased resistance to elevated catecholamine and calcium levels, reperfusion paradox. This study attempted to reproduce the phenomenon without applying any stress, but using a course of transauricular electric acupuncture. The isolated hearts of rats undergoing a course of the acupuncture were ascertained to show a clear-cut high resistance to the reperfusion paradox. After coronary ligation, the extent of necrosis in the animals having the acupuncture was significantly lower, as in those adapted to stress. The assumption that the phenomenon forming the basis for cardioprotective effects develops with electric acupuncture is discussed in the paper.

Adaptation, Physiological↗
PubMed1991

[Effects of adaptation to stress exposure and periodic hypoxia on bioelectric activity of cardiomyocytes of isolated heart in ischemia and reperfusion].

Action potential (AP) of cardiomyocytes was recorded in experiments on isolated perfused according to Langendorf rat hearts. The effect was estimated of preliminary adaptation to intermittent hypobaric hypoxia or to repeated short-term stress exposure on the resting potential (RP) and the amplitude and duration of action potential (APD) in global ischemia and reperfusion. It was shown that adaptation to hypoxia is more effective in prevention of ischemic fall of RP, AP and APD. In reperfusion, the parameters enumerated restored more quickly and efficiently in hearts from adapted to stress animals.

Action Potentials↗
PubMed1991

[Bioelectrical mechanism of the anti-arrhythmia effect of a synthetic acetylcholine analog EDIHYP].

The synthetic acetylcholine analogue ethyl-3-(2,2-dimethyl-2-ethyl-hydrazinium) propionic iodide (EDIHYP) exerts a powerful antiarrhythmic action in cardiac ischemic, reperfusion, and adrenergic lesions, as well as in infarction and postinfarction cardiosclerosis, as evidenced by animal experiments. The study was undertaken to examine the electrophysiological mechanism of EDIHYP s action on isolated rat heart cardiomyocytes. It was shown that the agent substantially reduced the resting potential, as well as action potential amplitude and duration in total ischemia and resultant reperfusion. The antiarrhythmic changes provided a multiple decrease in the duration of ventricular tachycardia and cardiac fibrillation in reperfusion. Thus, the fact that EDIHYP has a direct action on the bioelectrical activity of cardiomyocytes may play an important role in its antiarrhythmic effect in the whole body.

Animals↗
PubMed1991

[Adaptation of the body to stress effects increases resistance of nuclear DNA of cardiac cells due to accumulation of heat shock proteins in the nucleus].

It was shown that adaptation to stress exposure increased the resistance of nuclear DNA in myocardial cells to the damaging action of exogenous one-chain DNA (50 micrograms/ml). This protective effect was accompanied by a pronounced accumulation of heat shock proteins (hsp) 70 in nucleoplasm of myocardial cells from adapted animals. Possible mechanism of the DNA protective effect of adaptation and the role of hsp 70 are under discussion.

Adaptation, Physiological↗