The effects of single 1-hour immobilization stress exposure and of long-term (40 days) adaptation to intermittent high altitude hypoxia (in hypobaric chamber at "altitude" 4000 m, 4 hr, a day) on serum myoglobin content were studied in Wistar rats. It has been shown that such stress exposure induced the 2.5 fold increase in the serum myoglobin content. The adaptation did not change the myoglobin content, but effectively limited mentioned above stress-induced increase in the serum myoglobin level. These data suggest that serum myoglobin content can be used as a criterion for stress damage and efficiency of factors protecting against stress damage.

Acute Disease↗

PubMed1993

[Correction of disorders of cardiac electric stability in post-infarction cardiosclerosis using a diet enriched with polyunsaturated fatty acids].

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↗

PubMed1993

[Primary stress-induced myocardial disorders and arrhythmic heart disease. Part I].

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Adaptation, Physiological↗

PubMed1993

[Primary stress-induced myocardial injury and cardiac arrhythmia. Part II].

1. Heart injuries in single severe stress manifesting themselves primarily in disturbances of membrane lipid bilayer, sarcolemmal Na, K-pump and sarcoplasmic Ca-pump. At the same time there appear limited disturbances of the heart energy supply, namely, of creatine kinase system and glycolysis system. These disturbances cause small-focal myocardial lesions, lead to disorders of myocardium stretchability (poststress rigidity) and reduce the cardiac electrical stability: fibrillation threshold falls and ectopic activity increases. This complex of injuries is reversible to a considerable extent, but in repeated stress, the above mentioned damages localized mainly in richly innervated conduction system accumulate to cause even more pronounced disturbances of electric stability and severe arrhythmias. 2. Severe stress and beta-adrenergic effects on the heart regularly result in coronary vasodilation and increased coronary blood flow. However, the entire primary complex of stress-induced injuries and disturbances of the heart electric stability occur in this process despite the increased coronary blood flow. This corresponds to a well-known fact that isoproterenol, a selective beta-agonist, dilates blood vessels and simultaneously provokes a complex of injuries in the heart similar to the stress-induced one. Thus beta-adrenergic stress-induced injuries may indeed develop as primary stress damage to cardiomyocytes without any relation to ischemia. 3. The main factor determining a high vulnerability or, on the contrary, resistance of the heart to stress is the state of stress-limiting systems, namely, opioidergic, GABAergic, cholinergic, adenosinergic and other ones. Activation of these systems by adaptation to repeated stress or some other factors prevents serious injuries of the heart in severe stress.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗

PubMed1993

[Development of super-resistance to hypoxic hypoxia during adaptation to short-term stress].

Adaptation to intermittent short-term immobilization stress exposure increases the resistance of rats to hypoxic hypoxia. This was evidenced by the fact that in acute experiments in respiration with gas-mixture containing 6% of oxygen, the mortality of control rats was 65% compared with 10% of that of adapted rats. It has been estimated that this protective cross-effect of adaptation to stress is due to more stable and efficient mobilization of external respiration in adapted animals, and to a greater extent, to the fact that adapted rats tissues have gained a capacity of extracting more oxygen from hypoxemic blood compared to control animals. The role of previously stated phenomenon of adaptive stabilization of structures in superresistance to hypoxic hypoxia is discussed.

Adaptation, Physiological↗

PubMed1993

[Decrease in constrictor response and increase in dilator response of the resistant artery in experimental myocardial infarction: effect of adaptation to hypoxia on this phenomenon].

After adaptation to hypoxia experimental myocardial infarction does not result in enhanced vasodilatory responses of isolated tail artery from rat to acetylcholine and isoproterenol. At the same time the vascular reactivity to norepinephrine and phenylephrine is enhanced. These data may explain the previously described improvement in postinfarction time course of the blood pressure due to preliminary adaptation to hypoxia.

Adaptation, Physiological↗

PubMed1993

[Correlation between the antihypoxic effect of adaptation to stress and the course of electrostimulation].

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Adaptation, Physiological↗

PubMed1993

[Adaptation to periodic hypoxia decreases vasoconstrictor and increases vasodilator responses of resistant arteries].

Adaptation to intermittent hypoxia resulted in reduced vasoconstrictor responses of rat tail artery elicited by sympathetic nerve stimulation due to desensitization of alpha- and activation beta 2-adrenoceptors. Endothelium-dependent relaxation was enhanced under the impact of adaptation to intermittent hypoxia. These shifts may play a part in antihypertensive effect of adaptation to hypoxia which has been proved earlier.

Acetylcholine↗

PubMed1993

[Effect of fish oil with a high content of polyunsaturated fatty acids (eiconole) on myogenic tone and magnitude of the constrictor and dilator responses in isolated tail artery of rats].

A long-term excess of polyunsaturated fatty acids in diet resulted in more than twofold reduced myogenic tone of isolated rat tail artery. Vasoconstrictory responses to norepinephrine and phenylephrine were reduced as well. At the same time the excess of dietary polyunsaturated fatty acids resulted in enhanced vasodilatory responses to isoproterenol and acetylcholine. This complex of universally targeted shifts may play a significant part in the antihypertensive effect of excessive polyunsaturated fatty acids in diet.

Acetylcholine↗

PubMed1993

[The effect of a diet enriched with polyunsaturated fatty acids on the state of the Ca-transport system in the myocardial sarcoplasmic reticulum].

It was studied the influence of diet enriched with PUFA on the level of lipid peroxidation (LP) and rate of Ca-transport of sarcoplasmic reticulum (SR) of heart. The initial myocardial level of products of LP after the diet enriched with PUFA was two times higher than in control and this was associated with uneffected rate of Ca-transport. When kinetic analysis of myocardial Ca-transport with different concentration of Ca and process of autolysis were effectuated we could'nt show qualitative changes of state of Ca-transport system during diet with PUFA. For estimation of this effects comparison of two process were carried out--the increase of LP products and inhibition of Ca-transport of SR during LP induction in vitro. We shown, that after died enriched with PUFA identical level of LP products was accompanied with 3.5 times higher rate of inhibition of Ca-transport. As a result, we can say, that diet enriched with PUFA lead to considerable increase of resistance of Ca-transport system for LP induction and for high level of its oxidative products. The repeated compensated activation of LP was connected with adaptive effect, which could support the basic level of rate of Ca-transport. The mechanisms of these effect were discussed and comparison with adaptation for hypoxia was carried out.

Animals↗

PubMed1993

[The biphasic nature of the phenomenon of structural adaptational stabilization during the long-term adaptation of the body to stress].

During long-term (28 days) adaptation of the body to stress, the structural adaptational stabilization phenomenon (SASP) has a marked two-phase pattern: (1) SASP formation during nearly 14 days when protein transcription in heat shock was activated, hsp 70 was substantially accumulated and cardiac resistance to reperfusion damage drastically increased and (2) SASP reduction occurring despite continuous adaptation. By day 28 myocardial adaptation showed only two hsp 70 isoforms of the five revealed on day 14 of stress adaptation. Correspondingly, by day 28, the anticontractural effect of adaptation and its capacity of retaining the high contraction amplitude turned out to vanish in reperfusion. Moreover, ventricular fibrillation and ventricular tachycardia were observed in the control animal hearts during reperfusion, whereas these arrhythmias were seen only in 25 and 50% cases on days 14 and 28, respectively.

Adaptation, Physiological↗

PubMed1993

[The generalized accumulation of stress proteins during body adaptation to stress exposures].

It has been found that accumulation of stress proteins during adaptation to immobilization stress occurs not only in the heart, but in the brain (2 isoforms in the cytoplasm and 2 in the nucleus) and in the liver (1 isoform in the cytoplasm and 1 in the nucleus of hepatocytes). Thus, in heat shock the activation of protein synthesis is generalized during the body's adaptation to stress. This may underlie the generalization of the structural adaptational stabilization phenomenon and the formation of an adaptative defense of the whole organism.

Adaptation, Physiological↗

PubMed1993

[Ca2+ transport by the skeletal muscle sarcoplasmic reticulum in rats after suspension of the hindlimbs].

The functional capacity of skeletal muscle SR was examined in the lateral gastrocnemius (LG) of rats submitted to 1-40-day of disuse produced by a hindlimb suspension (HS). The Ca uptake by SR was measured in homogenate of muscle by means fo Ca-selective electrode, and the time course of SR Ca(2+)-pump inactivation in tissue homogenates incubated at 45 degrees C was studied. There were po significant effects of hindlimb unweighting on muscular Ca pump during 1-14 days of HS. The amount of Ca uptake in SR of LG was about 41% higher in the HS group than in the control after 25 days of HS. After 40 days of HS, the activity of Ca(2+) transport increased by 58% in SR atrophied HS muscle compared with the control. The increased resistance of LG muscle SR Ca pump to thermal exposure was observed after HS. The possible reasons of muscular Ca-pump activation after HS were discussed.

Animals↗

PubMed1993

[The antimutagenic effect of adaptation to stress].

C57BL mice were adapted to moderate periodic hypoxia and repeated electric pain stresses of limited intensity. These animals adapted to each of the factors and control animals were given the potent mutagen, free radical oxidation activator dioxidine in a single dose of 300 mg/kg. Dioxidine administered to unadapted animals resulted in chromosomal aberrations in 11% of stem bone marrow cells mainly due to the appearance of single and multiple chromosomes. Preadaptation to stress decreased the number of these dioxidine-induced chromosomal aberrations nearly twice. Adaptation to periodic hypoxia had no defensive action. As previously shown, adaptation to repeated stresses leads to the accumulation of heat-shock proteins (HSP) in the cellular nuclei of animals and prevents the degradation of isolated nuclei when single-chain DNA is added. Adaptation to hypoxia does not cause nuclear accumulation of HSP or prevents their degradation when unicellular DNA is supplemented. This suggests that the antimutagenic effect of stress adaptation is likely to be accounted for by the stabilizing action of HSP.

Adaptation, Physiological↗