Biomedical subjects
Publications and source records attributed to L Iu Golubeva.
Thyroid hormones seem to activate some fundamental cellular protective mechanisms and thus to be an important regulatory factor for local myocardial systems in their stress-limiting activity.
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A potent sound stimulation induces in Krushinskiĭ-Molodkina rats epileptiform seizures associated with increased blood levels of stressor hormones and subdural hemorrhages in the brain. Adaptation to periodic hypoxia carried out in a pressure chamber prolonged twofold the latent period of seizure development and blood hydrocortisone content after seizures. Such adaptation reduced the incidence of subdural hemorrhages and the mean size of these hemorrhages. Adaptation scheme used in our experiments is virtually the same as that clinically used at present in the management of patients with allergic diseases and neuroses.
Wistar male rats were adapted to intermittent hypoxia in an altitude chamber (group 1) and to short-term immobilization stress (group 2). The animals of both series and control ones were exposed to severe hypoxic hypoxia in acute experiment: they were anesthetized and inhaled a gas mixture which contained 6% O2. In the first two hours of the experiment the death rate was 65% in control, 10% in adaptation to stress, and 29% in adaptation to hypoxia. Principal parameters of respiration, circulation, and basic-acid equilibrium were monitored during the experiment. They allowed us to establish that both the variants of adaptation increased the tissue oxygen consumption; furthermore, adaptation to hypoxia preserved a higher level of oxygen consumption than adaptation to stress. Despite this, in adaptation to stress the death rate was threefold higher than in adaptation to hypoxia. This result was explained by the accumulation of heat shock proteins in cells during adaptation to stress and the resultant development of a phenomenon of adaptive stabilization of structures (PhASS). In adaptation to hypoxia the PhASS did not develop.
Adaptation to stress was produced by eight immobilizations of rats for 1 hour every other day. The effects of 25-min ischemia and subsequent 50-min reperfusion on the heart contractile function and energy metabolism were studied. In the adapted rats, the velocities of contraction and relaxation as well as the developed pressure restored during reperfusion much faster than in the controls. The NMR-study showed that a drastic fall of creatine phosphate (CP) and ATP during ischemia was followed by a rapid CP restoration, a Pi drop and a slow ATP restoration during reperfusion. In the adapted animals, the CP restoration was twice as rapid as in the controls. It is obvious that in adaptation to stress the heart function and the system of CP resynthesis appear to be significantly more resistant to ischemia stroke and this is why they restore their activity faster than in the controls.
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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.
The effect of preliminary adaptation to intermittent (40 days, 4 hrs daily at 4000 m "altitude") on the resistance of myocardial energy metabolism and contractile function to acute anoxia and subsequent reoxygenation was studied. It was found that adaptation to hypoxia significantly accelerated the restoration of creatine phosphate, ATP and creatine phosphokinase activity in myocardium in reoxygenation following acute anoxia. On the whole, this effect reduces the competition of H+ with Ca2+ in myofibrils to improve the energy supply and to accelerate the restoration of myocardial contractile function in reoxygenation.
Effect of preliminary adaptation to immobilization stress with progressive duration from 15 min. to 1 h (every second day, 8 sessions) on the resistance of indices of myocardial energy metabolism and contractile function to acute hypoxic hypoxia and subsequent reoxygenation was studied. It was shown, that adaptation to short-term stress exposure by some way provided the retention of activities of important enzymes like creatine-phosphokinase and phosphorylase under the harmful action of acute hypoxia and subsequent reoxygenation. At the same time, the ATP restoration and the CP super-restoration were observed during reoxygenation. This effect, in its turn, was accompanied by a more pronounced super-restoration of the heart contractile function than in control.
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The effect of preliminary administration of antioxidant ionol on the heart energy metabolism and contractile function was estimated in hypoxic hypoxia and subsequent reoxygenation. The protective effect of ionol on the energy metabolism in hypoxia was shown to occur mainly at the level of glycolysis. In reoxygenation, the protective effect of ionol manifested at the level of creatine kinase system to provide a rapid restoration of the CP synthesis rate. This shift correlated with the velocity of restoration of the developed pressure and the velocities of contraction and relaxation. On the whole the data obtained correspond to the notion that creatine kinase system and ATP play an important role in the depression and subsequent restoration on the heart contractile function in acute hypoxia and reoxygenation and ionol provides more effective performance of this system and correspondingly more rapid restoration of the contractile function in reoxygenation.
The rate of DNA reparative synthesis was studied in the nucleus of myocardial cells in the heart compensatory hyperfunction (HCH) induced by the aorta coarctation and in animals exposed to surgical stress without the aorta coarctation. It was established that both surgery and emotional painful stress activated the DNA reparative synthesis in myocardial cells. For example, 12-24 hrs following the surgery the DNA reparation rate exceeded control values by 50-74%. HCH induced no changes in the DNA reparation rate in nuclei of myocardial cells. The mechanism of stress-induced DNA damage is discussed and a hypothesis is put forward on stabilizing the effect of hyperfunction on the DNA structure.
A study of the effect of extreme physical stress on the contractility of an isolated heart, its CPK loss associated with anoxia and reoxygenation, and myocardial adenyl components and lactate levels under acute overstrain of the heart achieved through a complete obstruction of the aorta, showed the animals doing exercise to have reduced cardiac contractility, increased perfusate CPK waste, and sharply decreased myocardial macroergic phosphate levels under acute overstrain by pressure. Pretreatment with ionol largely prevented these changes.
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Rats with compensatory hypertrophy of the heart and control animals were subjected to emotional painful stress (EPS). It was established that EPS led to the lowering of the main indicators of the contractile function of an isolated papillary muscle and reduced the resistance of the function under study to excess/Na+ and H+ forcing out Ca2+ from the binding sites on the sarcolemma. Compensatory hypertrophy of the heart itself was accompanied by a reduction of the myocardial contractility but the increase of the concentration of Na+ and H+ in the perfusate led to a far greater depression of the contractile parameters than in the myocardium of the control animals. Contractile function of the hypertrophied myocardium after stress turned out to be reduced to the level close to that seen in heart insufficiency.
Emotional-pain stress results in a 25% decrease in Na K-ATPase activity in the heart. Injection of beta-adreno-blocker inderal in a dose of 1 mg/Kg bw 10 minutes before exposure to stress completely averts and decrease in the enzyme activity. This effect of inderal may be due to the inhibition of catecholamines which release in abundance during emotional-pain stress and which can indirectly damage the sarcolemma by means of lipid peroxidation activation.
A study was made of the effect of preadministering a water-soluble antioxidant (HP-6) belonging to th hydroxypyridine series on the development of hypoxic contracture and stressor heart injury. It was found that under hypoxia, the control animals and those exposed to emotional and pain stress develop characteristic heart contracture manifested by a rise in the diastolic pressure up to 40-47 mm Hg, as well as an abrupt increase in creatine phosphokinase egress from injured myocardial cells into perfusate. Administration of HP-6 to the animals for 3 days before stress and heart removal prevented to an appreciable degree the heart contracture and creatine phosphokinase egress. Also it made the recovery of contractility more rapid and complete during reoxygenation. It should be noted that in the animals which received HP-6 before stress, the contractility got recovered to a far greater extent than that in the controls. The evidence obtained suggests an important role played by activation of lipid peroxidation in the pathogenesis of hypoxic contracture and reoxygenation-induced heart injury.