Abstract
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.
Highlights
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
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
При экспериментальном адреналиновом повреждении в сердечной ткани крыс с трансплантацией неонатальных, ксеногенных сердечных клеток значительно уменьшается развитие анаэробных условий с ограничением накопления лактата в ранние сроки
Summary
К механизму адреналинового повреждения сердечной ткани и механизму кардиопротекции неонатальными, ксеногенными, сердечными клетками. динамика креатинфосфата, лактата и малонового диальдегида. Креатинфосфата и лактата в сердечной ткани крыс при экспериментальном адреналиновом стрессе и при его коррекции неонатальными, ксеногенными, сердечными клетками. Что скачок уровня малонового диальдегида и, соответственно, активация свободнорадикальных процессов при адреналиновом повреждении сердца происходили в период перестройки энергетики сердечной клетки с интенсивного гликолиза к восстановлению активного митохондриального синтеза АТФ (что соответствовало окончанию истощения лактата и креатинфосфата и началу восстановления их содержания в сердечных клетках). Полученные данные свидетельствует о том, что трансплантация неонатальных сердечных клеток в условиях адреналинового стресса способна ограничивать нарушение аэробных и анаэробных процессов в сердечной ткани, содействовать восстановлению митохондриальных энергетических процессов, при этом способствуя более эффективному и щадящему восстановлению митохондриального синтеза АТФ, сопровождающемуся меньшим всплеском повреждающих свободнорадикальных процессов. Irkutsk Scientific Centre of Surgery and Traumatology (Bortsov Revolyutsii str. 1, Irkutsk 664003, Russian Federation)
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