MITOCHONDRIA RESPIRATION IN RAT BRAIN NEURONS UNDER CEREBRAL ISCHEMIA OF VARYING SEVERITY
The knowledge of the mechanisms of energy deficiency development in ischemic lesions is necessary to specify the pathogenesis and assess the damage/compensation ratio. The aim of the paper is to study respiration indices of mitochondria of rat brain homogenates in total and subtotal cerebral ischemia. Materials and Methods. The experiments were carried out on 88 male outbred white rats weighing 260±20 grams in compliance with the Directive 2010/63/EU of the European Parliament and of the Council of 22 September 2010 on the protection of animals used for scientific purposes. Results. In 1-hour subtotal cerebral ischemia, V2 increased by 24 (18; 27) % (p0.05). In the presence of malate/glutamate under 1-hour SCI, mitochondrial respiration rates V1, V2, V3, and V4 were higher than under 1-hour TCI 89 (82; 93), 58 (55; 63), 24 (21; 29) and 32 (27; 37) % respectively (p<0.05). Decrease in V1, V2, and V3 indices under 24-hour SCI is a consequence of the decrease in oxygen content for mitochondrial respiration. The inhibition of energy processes is more pronounced than under 1-hour SCI, which reflects the extremely low phosphorylation coefficient. Changes in V1, V2, and V3 indices under 1-hour SCI and 1-hour TCI are multidirectional. Their increase under SCI is associated with uncoupling between oxidation and phosphorylation, while their decrease under TCI is associated with a lack of substrates for mitochondrial respiration. Conclusion. The most pronounced decrease in respiration indices of the mitochondrial fraction of brain homogenates occurs under total cerebral ischemia due to the complete cessation of neuron blood supply.