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.     

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.     

Structural changes in the rat myocardium in the process of adaptation to high-altitude hypoxia]

Changes in the weight of diverse parts of the heart, in cross-sectional area of myocytes and vascularization of the myocardium were studied in rat experiments under altitude hypoxia (3200 m above the sea level) during adaptation of the animals to hypoxia. Morphologically, the compensatory and adaptive reactions of the rat to hypoxia were shown by its increases weight at the expense of hypertrophy of the right ventricular myocardium. Vascularization of the myocardium augmented synchronously to its growing hypertrophy.     

Effects of adaptation to periodic and continuous hypoxia in disorders of electrical stability of the heart in postinfarction cardiosclerosis

The effects of adaptation to intermittent and continuous hypoxia on the electrical stability of the heart were compared in middle altitude conditions and in altitude chamber in Wistar rats with postinfarction cardiosclerosis. It has been shown that both forms of adaptation could restore the heart fibrillation threshold and restrict the ectopic activity in postinfarction cardiosclerosis. Beneficial effects of adaptation to intermittent hypoxia in conditions of the altitude chamber appeared to be more radical.     

Alpha1 desensitization of the heart during adaptation to stress]

Results of the experiments evidence that a combination of three factors, limiting the Ca2+ concentration increase in myocardial cell, can play a role in the cardioprotective effect of adaptation of rats to short-term immobilization stress (every second day for a month) are presented. Those factors are as follows: desensitization of alpha 1-adrenoreceptors, M-cholinoreceptors up-regulation and reduced number of voltage-dependent Ca2+ channels in the myocardial membranes.     

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.     

Neurohumoral mechanisms of the rat heart adaptation to overload

The present study confirms involvement of the sympathicoadrenal system in adaptation of heart to overload. Besides, at formation of chronic heart failure (CHF) there have been revealed a rise of the histamine and serotonin levels in blood plasma and myocardium as well as glucocorticoid hyperactivation.     

The role of malate dehydrogenase in adaptation to hypoxia in invertebrates]

In muscle tissue of lamellibranch molluscs and crustaceans (cf. Table for the species studied), high levels of malate dehydrogenase and low ones of lactade dehydrogenase were detected. There is a direct relationship between the value of MDH/LDH ratio and the capacity of organisms to withstand temporary anaerobiosis. Animals with high ratio may adapt to hypoxia by transition from aerobic metabolism to anaerobic one.     

Prevention of the depression of normal killer activity in stress via adaptation to the periodic action of hypoxia

It has been demonstrated that progressive adaptation of BALB/c mice for 28 days to periodic action of pressure chamber hypoxia prevents the stress-induced depression of normal killer activity. Moreover, preadaptation to hypoxia reverses the stress-provoked inhibition of DNA synthesis in the thymic and spleen cells.     

Participation of heart prostaglandins in cardioprotective cross-effects of adaptation to stress and hypoxia

An adaptation to stress and hypoxia was found to increase the baseline PGE content in the myocardium. The data obtained suggest that the activation of the myocardial system of protective PGs is an important link in the cardioprotective effects of adaptation.     

Growth of cardiac muscle cells during rat adaptation to altitude hypoxia

The weight of the right heart ventricle in 1.5-month-old rats kept after birth in the mountains of 3400 m altitude is higher and its muscle cell cytoplasm mass is much larger compared to those in 1.5-month-old animals raised at 800 m altitude. The hypertrophy of cells is not due to their polyploidization. Only a small increase in the relative number of polyploid cells takes place under high altitude hypoxia. The weight of the right ventricle and myocyte mass in 3-month-old rats kept 1.5-3 months after the birth at 3400 m altitude also increases, although this augmentation is significantly less than in the animals grown in the mountains for 1.5 months immediately after the birth. The myocyte ploidy of adult animals adapted to hypoxia does not essentially differ from that of 1.5- and 3-month-old control rats: about 80 per cent of these cells are polyploid. Thus, the growth of cardiac myocytes under the heart hyperfunction in the case of high altitude hypoxia proceeds mainly on the ground of the stable polyploid genome, as well as normal ontogenetic growth of these cells.     

Effect of adaptation to periodic hypoxia on post-infarction fall of blood pressure and hyperactivation of the endothelium

Acute stress concomitant to the experimental myocardial infarction has induced endothelial hyperactivation of the rat aorta exhibited in an increase of inhibition of norepinephrine-induced contractions of vascular smooth muscle, enhanced endothelium-dependent relaxation correlating with a fall of systemic blood pressure. Preliminary adaptation of rats to intermittent hypobaric hypoxia greatly prevented the stress-induced endothelial hyperactivation and beneficially affected the postinfarction time course of blood pressure.     

The protective effect of carnosine in hypoxia and reoxygenation of the isolated rat heart]

The effect of carnosine (15 mM) on the contractile activity of isolated rat hearts contracting in an isotonic regime (37 degrees C at a 5 Hz stimulation frequency) has been studied. Carnosine added to the perfusing solution had no effect on the contractile activity either in hypoxia or during reoxygenation but decreased it with a simultaneous increase in the coronary flow during reoxygenation. Carnosine inhibited by 60% the lactate dehydrogenase release from cardiac cells. A conclusion is drawn that the protective effect of carnosine is due to its membrane-stabilizing action which is implemented during inhibition of peroxidation of membrane lipids.