PECULIARITIES OF ACTIVATION OF LIPID PEROXIDATION PROCESSES IN THE EARLY PERIOD OF CRANIOSKELETAL INJURY COMPLICATED BY BLOOD LOSS IN RATS WITH DIFFERENT RESISTANCE TO HYPOXIA
DOI:
https://doi.org/10.11603/mcch.2410-681X.2020.v.i3.11547Keywords:
cranioskeletal trauma, blood loss, resistance to hypoxia, lipid peroxidationAbstract
Introduction. Injury is one of the current problems. Its structure is dominated by a combined craniocerebral and skeletal trauma, which is accompanied by the highest mortality. One of the markers of traumatic disease is the intensification of lipid peroxidation in tissues and organs, which underlies the pathogenesis of multiorgan failure. Under these conditions, the patterns of lipid peroxidation processes in individuals with different resistance to oxygen deficiency remain virtually unexplored.
The aim of the study – to determine the peculiarities of the activation of lipid peroxidation in the early period of cranioskeletal trauma complicated by blood loss in rats with different resistance to hypoxia.
Research Methods. The experiments were performed on 148 nonlinear white male rats weighing 180–200 g, which were on the standard diet of the vivarium. Previously, individual resistance to hypoxia was determined in rats and two groups were identified: high- and low-resistance. In animals, cranioskeletal trauma was simulated and combined with acute blood loss. After 1, 3 and 7 days in the liver of animals resistant to hypoxia, the content of reagents for thiobarbituric acid was determined – a screening marker of lipid peroxidation intensification.
Results and Discussion. In response to cranioskeletal trauma in experimental animals there is an activation of lipid peroxidation of cell membranes of hepatocytes. Under conditions of additional blood loss, there is a layering of the influence of pathogenic mechanisms of trauma and hypoxemia, in which there is an increase in the formation of reagents in the liver to thiobarbituric acid. In highly resistant animals to hypoxia, the degree of accumulation of reagents for thiobarbituric acid in the liver was significantly lower than in low-resistant animals at all times. The obtained results indicate that in highly resistant animals, despite the higher intensity of lipoperoxidation in the initial state, the reaction to trauma is accompanied by less activation of lipid peroxidation processes than in low-resistant animals. This suggests a lower probability of developing multiorgan failure in highly resistant animals, which is of great practical importance and requires further study.
Conclusion. In response to cranioskeletal trauma and its combination with acute blood loss in the acute period and the period of early manifestations of traumatic disease compared with control, there is an increase in the intensity of lipid peroxidation in the liver of highly and low hypoxia-resistant animals.
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