FEATURES OF TISSUE RESPIRATION DISTURBANCES IN ANIMALS WITH EXPERIMENTAL TRAUMATIC BRAIN INJURY COMBINED WITH DIABETES

Background. Based on statistics for overall traumatism, traumatic brain injury (TBI) contributes 30–50% cases and causes an annual death of 1.5 million and disability for more than 2.4 million people in the world. Modern ideas about the pathogenesis of cranial trauma based on the allocation of primary and secondary factors of brain damage. One of the main causes of the secondary brain injury is hypoxia — insufficient oxygen supply. Indicators of blood gas composition are important criteria for evaluating the degree of metabolism in diabetes.

Objectives. Identify changes in oxygen balance and carbohydrates metabolism in experimental traumatic brain injury in combination with diabetes mellitus.

Methods. Rats were subjected to the cranial injury on the background of streptozotocin-induced diabetes. After 3, 24 hours, 5 and 14 days after the onset of the injury, values of oxygen balance, lactic and pyruvic acid were measured in the blood.

Results. While analyzing the state of respiration after TBI, we found reduced hemoglobin saturation of arterial and venous blood oxygen, reduced total oxygen content in arterial and venous blood, increased arteriovenous difference in oxygen consumption rate of oxygen by tissues, and increased the coefficient of oxygen utilization rate. At the same time we observed decrease in tissue oxygen consumption rate and tissue respiration intensity that pointed to significant overstrain of transport and oxygen consumption mechanisms. Moderate tissue hypoxia in the early period after injury is accompanied by excessive formation of lactic and pyruvic acids and increased ratio of lactate/pyruvate.

Conclusions. In TBI with the background of diabetes, we observed significant overstrain mechanisms of transportation and consumption of oxygen, resulting in insufficient oxygenation of tissues which was accompanied by severe decompensation of aerobic metabolism of carbohydrates.