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.