To the Mechanism of Adrenaline Damage to the Heart Tissue and the Mechanism of Cardioprotection by Neonatal, Xenogenic, Cardiac Cells. Dynamics of Creatine Phosphate, Lactate and Malondialdehyde

The development of disturbances in energy processes and damaging free radical reactions in various pathological processes, including cardiovascular diseases, are interrelated and lead to a significant deterioration in the course of diseases.Aim of the study. Research of the dynamics of malondialdehy...

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Main Authors: S. L. Bogorodskaya, A. A. Runovich
Format: Article
Language:Russian
Published: Scientific Сentre for Family Health and Human Reproduction Problems 2021-01-01
Series:Acta Biomedica Scientifica
Subjects:
Online Access:https://www.actabiomedica.ru/jour/article/view/2526
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author S. L. Bogorodskaya
A. A. Runovich
author_facet S. L. Bogorodskaya
A. A. Runovich
author_sort S. L. Bogorodskaya
collection DOAJ
description The development of disturbances in energy processes and damaging free radical reactions in various pathological processes, including cardiovascular diseases, are interrelated and lead to a significant deterioration in the course of diseases.Aim of the study. Research of the dynamics of malondialdehyde, creatine phosphate and lactate in the cardiac tissue of rats under experimental adrenaline stress and during its correction with neonatal, xenogenic, cardiac cells.Methods. The experiment was carried out on outbred male rats. Adrenaline damage to the heart was simulated by a single subcutaneous injection of 0.1% adrenaline solution at a dose of 0.5 mg per 100 g of body weight. The first group (37 rats) was injected subcutaneously with adrenaline, the second group (41 rats) – adrenaline and isolated heart cells of a newborn rabbit at a dose of 500 000. The third group included 6 healthy rats.Results. It was found that a spike in the level of malondialdehyde and, accordingly, the activation of free  radical processes in adrenaline damage to the heart, occurred during the restructuring of the energy of the  heart cell from intense glycolysis to the restoration of active mitochondrial ATP synthesis (which corresponded to the end of the depletion of lactate and creatine phosphate, and the beginning of the restoration of their content in heart cells).  The dynamics of MDA sensitively reflected both the activity and the inhibition of oxidative processes in mitochondria, which manifested itself, respectively, both in the form of peaks and in a low level of MDA and corresponded to the interpretation of the dynamics of lactate and creatine phosphate.In the cardiac tissue of rats with transplantation of neonatal, xenogenic cardiac cells, the accumulation of lactate in the early stages of the experiment decreased, the subsequent depletion of the cellular reserves of creatine phosphate and lactate was inhibited, the period of inhibition (non-increase) in MDA was shorter, the subsequent increase in MDA was more moderate than in control animals.Conclusion. The data obtained indicate that neonatal cardiac cells are able to limit the disturbance of aerobic and of anaerobic processes in the heart tissue and promote the restoration of mitochondrial energy processes.  Moreover, they contribute to a more efficient restoration of mitochondrial ATP synthesis, accompanied by a smaller burst of damaging free radical processes.
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spelling doaj.art-18763dd814ed4523a1bdacc93ec42deb2024-03-28T07:49:24ZrusScientific Сentre for Family Health and Human Reproduction ProblemsActa Biomedica Scientifica2541-94202587-95962021-01-015626527010.29413/ABS.2020-5.6.352103To the Mechanism of Adrenaline Damage to the Heart Tissue and the Mechanism of Cardioprotection by Neonatal, Xenogenic, Cardiac Cells. Dynamics of Creatine Phosphate, Lactate and MalondialdehydeS. L. Bogorodskaya0A. A. Runovich1Irkutsk Scientific Centre of Surgery and TraumatologyIrkutsk Scientific Centre of Surgery and TraumatologyThe development of disturbances in energy processes and damaging free radical reactions in various pathological processes, including cardiovascular diseases, are interrelated and lead to a significant deterioration in the course of diseases.Aim of the study. Research of the dynamics of malondialdehyde, creatine phosphate and lactate in the cardiac tissue of rats under experimental adrenaline stress and during its correction with neonatal, xenogenic, cardiac cells.Methods. The experiment was carried out on outbred male rats. Adrenaline damage to the heart was simulated by a single subcutaneous injection of 0.1% adrenaline solution at a dose of 0.5 mg per 100 g of body weight. The first group (37 rats) was injected subcutaneously with adrenaline, the second group (41 rats) – adrenaline and isolated heart cells of a newborn rabbit at a dose of 500 000. The third group included 6 healthy rats.Results. It was found that a spike in the level of malondialdehyde and, accordingly, the activation of free  radical processes in adrenaline damage to the heart, occurred during the restructuring of the energy of the  heart cell from intense glycolysis to the restoration of active mitochondrial ATP synthesis (which corresponded to the end of the depletion of lactate and creatine phosphate, and the beginning of the restoration of their content in heart cells).  The dynamics of MDA sensitively reflected both the activity and the inhibition of oxidative processes in mitochondria, which manifested itself, respectively, both in the form of peaks and in a low level of MDA and corresponded to the interpretation of the dynamics of lactate and creatine phosphate.In the cardiac tissue of rats with transplantation of neonatal, xenogenic cardiac cells, the accumulation of lactate in the early stages of the experiment decreased, the subsequent depletion of the cellular reserves of creatine phosphate and lactate was inhibited, the period of inhibition (non-increase) in MDA was shorter, the subsequent increase in MDA was more moderate than in control animals.Conclusion. The data obtained indicate that neonatal cardiac cells are able to limit the disturbance of aerobic and of anaerobic processes in the heart tissue and promote the restoration of mitochondrial energy processes.  Moreover, they contribute to a more efficient restoration of mitochondrial ATP synthesis, accompanied by a smaller burst of damaging free radical processes.https://www.actabiomedica.ru/jour/article/view/2526xenogenic heart cellsadrenaline damagecreatine phosphatelactatemalondialdehyde
spellingShingle S. L. Bogorodskaya
A. A. Runovich
To the Mechanism of Adrenaline Damage to the Heart Tissue and the Mechanism of Cardioprotection by Neonatal, Xenogenic, Cardiac Cells. Dynamics of Creatine Phosphate, Lactate and Malondialdehyde
Acta Biomedica Scientifica
xenogenic heart cells
adrenaline damage
creatine phosphate
lactate
malondialdehyde
title To the Mechanism of Adrenaline Damage to the Heart Tissue and the Mechanism of Cardioprotection by Neonatal, Xenogenic, Cardiac Cells. Dynamics of Creatine Phosphate, Lactate and Malondialdehyde
title_full To the Mechanism of Adrenaline Damage to the Heart Tissue and the Mechanism of Cardioprotection by Neonatal, Xenogenic, Cardiac Cells. Dynamics of Creatine Phosphate, Lactate and Malondialdehyde
title_fullStr To the Mechanism of Adrenaline Damage to the Heart Tissue and the Mechanism of Cardioprotection by Neonatal, Xenogenic, Cardiac Cells. Dynamics of Creatine Phosphate, Lactate and Malondialdehyde
title_full_unstemmed To the Mechanism of Adrenaline Damage to the Heart Tissue and the Mechanism of Cardioprotection by Neonatal, Xenogenic, Cardiac Cells. Dynamics of Creatine Phosphate, Lactate and Malondialdehyde
title_short To the Mechanism of Adrenaline Damage to the Heart Tissue and the Mechanism of Cardioprotection by Neonatal, Xenogenic, Cardiac Cells. Dynamics of Creatine Phosphate, Lactate and Malondialdehyde
title_sort to the mechanism of adrenaline damage to the heart tissue and the mechanism of cardioprotection by neonatal xenogenic cardiac cells dynamics of creatine phosphate lactate and malondialdehyde
topic xenogenic heart cells
adrenaline damage
creatine phosphate
lactate
malondialdehyde
url https://www.actabiomedica.ru/jour/article/view/2526
work_keys_str_mv AT slbogorodskaya tothemechanismofadrenalinedamagetothehearttissueandthemechanismofcardioprotectionbyneonatalxenogeniccardiaccellsdynamicsofcreatinephosphatelactateandmalondialdehyde
AT aarunovich tothemechanismofadrenalinedamagetothehearttissueandthemechanismofcardioprotectionbyneonatalxenogeniccardiaccellsdynamicsofcreatinephosphatelactateandmalondialdehyde