In a 14-20 days after feeding of rats with "eikonole" (cod-liver oil, deduced from skeletal muscle and enriched by eicosapentaenic and docosahexaenic fatty acids). Myocardial infarction by Selie has been induced and in a 30 days of the same feeding, contractile function and heart electrical stability in situ have been investigated. Eikonole increased heart fibrillation threshold by 50%, decreased the frequency of spontaneous extrasystole in 3 times and ectopic activation (extrasystole), induced by n. vagus stimulation, in 2.5 times. Eikonole increased the intensity of structures' functioning in the state of relative physiological rest, but did not influence essentially on pressure and the velocity of myocardial contraction and weakening.

Animals↗

PubMed1992

Differences in adaptive stabilization of structures in response to stress and hypoxia relate with the accumulation of hsp70 isoforms.

The phenomenon of adaptive stabilization of structures (PhASS) develops during adaptation of the organism to intermittent restraint stress. The PhASS manifests itself in a considerably increased resistance of the heart to a broad spectrum of harmful factors. In the present work, the content of hsp70 and their role in the development of PhASS during adaptation to intermittent restraint stress and to intermittent hypoxia were studied. In adaptation to restraint stress, five hsp70 isoforms with pI ranging from 5.7 to 6.3 were accumulated in the myocardium. The heart simultaneously became strikingly resistant to reperfusion paradox and heat shock. In adaptation to hypoxia, only two hsp70 isoforms with pI about 5.8 were accumulated. The resistance to reperfusion paradox was not increased and the resistance to heat shock was increased only moderately. These data suggest a role of different hsp70 isoforms in the mechanism of PhASS as well as adaptive protection of the heart.

Adaptation, Physiological↗

PubMed1992

[The anti-arrhythmic efficacy of sodium valproate].

The antiarrhythmic efficacy of the anticonvulsant sodium valproate was studied in 22 patients with ventricular premature contraction in the immediate (10-15 days) and late (2-5 months) periods of therapy. The prolong antiarrhythmic effect of the drug was observed in 66% of the patients in whom it was beneficial in the first days of therapy. The results obtained provide strong evidence for the efficacy of sodium valproate in patients with ventricular premature contraction occurring in the presence of neurocirculatory dystonia.

Adolescent↗

PubMed1992

[The clinico-hemodynamic effects of the activator of the GABA-ergic stress-limiting system sodium valproate (acediprol) and etatsizin in patients with cardiac arrhythmias].

Hemodynamic and antiarrhythmic effects of acediprol and ethacizine were examined in 51 patients with premature ventricular contraction concurrent with neurocirculatory dystonia and coronary heart disease. It was ascertained that acediprol exerted a positive inotropic action and ethacizine lowered myocardial contractility. Acediprol therapy prevents or attenuates the hypokinetic and arrhythmogenic effects of stimulated stress in patients with ischemic and non-ischemic arrhythmias. The preventive antiarrhythmic effect of acediprol is the most pronounced in patients with neurocirculatory dystonia. Ethacizine fails to improve hemodynamic supply of the stress test and enhances stress-related hypodynamia in some patients.

Anti-Arrhythmia Agents↗

PubMed1992

[Role of the inositol phosphate cycle in the cardioprotective effect of adaptation to intermittent hypoxia].

The impact of adaptation to intermittent hypoxia of different duration (for 20 and 40 days) on the inositol triphosphate-diacylglycerol (ITP-DAG) regulatory contour in the heart was investigated. For this, isolated heart alpha 1-adrenoreactivity to phenylephrine and phospholipase (PhL-C) activities were studied in cardiac plasma membranes. On day 20 of adaptation, the heart inotropic response to phenylephrine stimulation was somewhat reduced and the activity of Ca(2+)-dependent PhL-C did not differ from that in the controls within the range of Ca2+ physiological concentrations. Forty days after adaptation, both positive inotropic responses of the heart to phenylephrine and activity of Ca(2+)-dependent PhL-C were enhanced, i.e. activation of the ITP-DAG regulatory cascade occurred. Early studies have shown that a phenomenon of adaptive stabilization develops at this stage of adaptation. The phenomenon appears as a significant increase in heart resistance to thermal injury, toxic catecholamine levels, Ca2+ paradox and high Ca2+ concentrations. Thus, the revealed activation of the ITP-DAG regulatory contour was accompanied by the development of a phenomenon of adaptive structure stabilization (PhASS) in the hearts of adapted animals. The findings suggest that the ITP-DAG regulatory cascade plays an important role in the cardioprotective effect of adaptation to intermittent hypobaric hypoxia and in PhASS formation.

Adaptation, Physiological↗

PubMed1992

[The role of the liver macrophage system in decreasing the immune complex level of the blood during adaptation to periodic hypoxia].

It has been established that adaptation to intermittent hypoxia in altitude chamber considerably increases the capacity of hepatic macrophagal systems (MFS) to uptake Indian ink particles from the blood as well as immunoglobulin labelled with fluorescein isothiocyanate. There is simultaneous catabolism of labelled albumin in hepatic MFS. It has been suggested that the increased C3b-component of complement system in blood observed in adaptation to hypoxia plays a substantial role in the activation of hepatic MFS. The role of hepatic MFS activation in reducing the number of circulating immune complexes is emphasized as well as its role in therapeutic effect of adaptation in allergic diseases.

Adaptation, Physiological↗

PubMed1992

[Adaptation to periodic hypoxia decreases ethanol consumption and abstinence-related damages to the internal organs during withdrawal in chronically alcoholized animals].

Adaptation to intermittent hypoxia in a hypobaric altitude chamber reduced two-fold ethanol consumption in chronically alcoholized rats and limited or eliminated abstinence syndrome. The effect of the adaptation was evident from prevented development of abstinence analgesia, enhanced alcohol consumption following deprivation, abstinence activation of lipid peroxidation in the liver, and release of hepato-specific enzymes fructose monophosphate and gamma-glutamyl transpeptidase into blood. At the same time adaptation prevented the fall of cardiac fibrillation threshold and pronounced disturbance of ventricular contraction and relaxation. The problem is discussed of using adaptation to intermittent hypoxia in the treatment for those forms of alcoholism in which abstinence plays the key role.

Adaptation, Physiological↗

PubMed1992

[Reversal of withdrawal injuries of the heart and liver by adaptation to intermittent hypoxia when discontinuing ethanol in chronically alcoholized animals].

Adaptation to intermittent hypoxia in the hypobaric altitude chamber showed a two-fold decrease in ethanol consumption in chronically alcoholized rats and attenuated or arrested the withdrawal syndrome. The impact of adaptation to the withdrawal syndrome was that it prevented the development of withdrawal analgesia, higher alcohol consumption after its withdrawal, withdrawal hepatic activation of lipid oxidation products and blood release of the hepatic specific enzymes fructose monophosphataldolase and gamma-glutamyl transpeptidase. Concurrently, the adaptation prevented the withdrawal fall of the cardiac fibrillation threshold and marked disorders of ventricular contraction and relaxation. The paper discusses whether adaptation to intermittent hypoxia can be used in the management of the types of alcoholism in whose development the withdrawal plays the key role.

Adaptation, Physiological↗

PubMed1992

[Increase of calcium-dependent activity of phospholipase C in the myocardium in adaptation of animals to short-term stress effects].

The effect of adaptation of rats to repeated short-term stress exposures was studied on the density and the affinity of alpha 1-adrenoceptors in the heart and on the phospholipase C activity and sensitivity to changes in Ca2+ concentration. It was found that adaptation to stress was accompanied by a desensitization of alpha 1-adrenoceptors and also by an increase in Ca(2+)-dependence of phospholipase C activity in the heart. The role of increased activity of phospholipase C and activated inositol triphosphate-diacylglycerol regulatory cascade is discussed as regard to the previously revealed accumulation of heat shock proteins in the myocardium and to the adaptive protection of the heart.

Adaptation, Physiological↗

PubMed1992

[Comparative anti-arrhythmia effectiveness of activators of body stress-limiting systems in patients with arrhythmia].

The antiarrhythmic effects produced by activators of the body's stress-limiting systems were comparatively evaluated in patients with cardiac arrhythmias of ischemic and non-ischemic etiology. Acediprol, gidazepam, and befol were found to be beneficial in ventricular premature contraction when psychoemotional stress was simulated, as evidenced by 24-hour monitoring. The most pronounced protective therapeutical effect of the drugs was observed in patients with arrhythmias of extracoronary origin and in individuals with a marked arrhythmogenic effect of stress. Gidazepam was shown to suppress the provocative arrhythmogenic effect of the stress test.

Adult↗

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↗