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Портал Begell Электронная Бибилиотека e-Книги Журналы Справочники и Сборники статей Коллекции
International Journal of Physiology and Pathophysiology
SJR: 0.116

ISSN Печать: 2155-014X
ISSN Онлайн: 2155-0158

Archives: Volume 1, 2010 to Volume 9, 2018

International Journal of Physiology and Pathophysiology

DOI: 10.1615/IntJPhysPathophys.v9.i2.10
pages 99-108

Oxidative Power and Intracellular Distribution of Mitochondria Regulate Cell Oxygen Regime under Circulatory Hypoxia

Katerina G. Liabakh
International Scientific Training Center for Information Technologies and Systems, National Academy of Sciences of Ukraine, Kyiv, Ukraine

Краткое описание

The regulatory impact of the mitochondria spatial distribution and enlargement in their oxidative power qO2 on oxygen consumption and the tissue oxygenation of a skeletal muscle during circulatory hypoxia were studied. Investigations were performed by mathematical modeling of O2 3D diffusion in a myocyte. The oxygen consumption rate (VO2) and intracellular oxygen tension (pO2) were analyzed at a moderate load against the background of reduced muscle blood flow in the range from 0.950 to 0.012 ml · min−1 · g−1, as well as in the case of an increase in the intercapillary distance from 0.0040 to 0.0064 cm. The cells with evenly (case 1) and unevenly (case 2) distributed mitochondria were considered. According to calculations, a rise in mitochondria oxidative power from 0.06 to 0.10 ml · min−1 · g−1 made it possible to maintain mean value of VO2 constant level (0.055 ml · min−1 · g−1) despite a decrease in O2 delivery. The growth of qO2 also controlled oxygen regime at high intercapillary distance. At even distribution of mitochondria (case 1), minimum value of tissue pO2 was less than 1 mm Hg, and an area of hypoxia appeared inside the cell. When mitochondria were distributed unevenly, pro-portionally to VO2 gradient (case 2), pO2 increased, exceeding the critical level. At that, hypoxia disappeared, and minimum value of pO2 increased from 0 to 4 mmHg. The possibilities of such regulation depend on the "blood flow-oxygen demand" relation. It has been assumed that an increase in mitochondrial enzyme activity and mitochondria migration to the places of the greatest oxygen consumption rate enables improving oxygen regime in native cells in terms of their adaptation to hypoxia.


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