DYNAMICS OF THE ENZYME LINK OF THE ANTIOXIDANT DEFENSE UNDER THE INFLUENCE OF ISCHEMIA-REPERFUSION OF THE LIMB, ACUTE BLOOD LOSS AND FRACTURE OF THE MANDIBLE
DOI:
https://doi.org/10.11603/mcch.2410-681X.2021.i1.12113Keywords:
fracture of the lower jaw, blood loss, turnstile, ischemia, reperfusion, liver, antioxidant protectionAbstract
Introduction. In the modern world, the prevalence of gunshot injuries complicated by acute blood loss from the extremities has increased significantly. The use of a hemostatic tourniquet under these conditions with a maximum period of 2 hours belongs to the main measures for rescuing the wounded on the battlefield. In the structure of gunshot injuries, despite injuries to the extremities, the frequency of injuries to the facial part of the skull increased significantly, with predominant damage to the lower jaw. In the pathogenesis of the systemic manifestations of these lesions, the leading role is played by the enhancement of lipid peroxidation processes. However, the effect of limb ischemia-reperfusion, acute blood loss and fracture of the lower jaw on the state of the enzyme link of antioxidant defense in the liver has been insufficiently studied.
The aim of the study – to elucidate the effect of acute blood loss, two-hour ischemia of the limb and trauma of the lower jaw on the dynamics of violations of the enzyme link of the liver antioxidant defense during the reperfusion period.
Research Methods. The experiments were performed on 146 nonlinear male rats weighing 200–220 g. All animals were divided into five groups: control and four experimental. In the first experimental group of animals, limb ischemia-reperfusion was simulated under thiopenthalonate anesthesia, acute blood loss (20 % of the circulating blood volume) in the second, and these lesions were combined in the third. In the fourth experimental group of animals with acute blood loss and ischemia-reperfusion of the limb, a fracture of the mandible was additionally simulated. After 2 and 3 hours, as well as after 1, 7 and 14 days, the animals were removed from the experiment and the activity of superoxide dismutase (SOD) and catalase was determined in the liver.
Results and Discussion. It was found that two-hour limb ischemia in the reperfusion period is accompanied by a significant decrease in SOD activity with a maximum after 1 day, which returns to the control level after 14 days. At the same time, during all periods of observation, the activity of catalase is increased, which is of a compensatory nature and indicates the appearance of reactive oxygen species in the liver. Under conditions of acute blood loss, the activity of antioxidant defense enzymes in the liver significantly decreases after 2 hours of the experiment, reaches a minimum after 1 day and increases up to 14 days, but does not reach the control level. Additional modeling of limb ischemia-reperfusion against the background of acute blood loss is accompanied by the greatest decrease in SOD and catalase values in the liver at all periods of observation, indicates a layering of pathogenic mechanisms of both interventions and indicates a significant increase in prooxidant mechanisms caused by organ hypoxia. Additional modeling of a fracture of the lower jaw against the background of acute blood loss and ischemia-reperfusion of the limb is accompanied by deepening violations of the enzyme link of antioxidant protection in the liver. A significantly lower level of SOD after 1 day and catalase after 1 and 7 days is noted compared to animals that were simulated with acute blood loss and ischemia-reperfusion of the limb, indicates an important pathogenic role of mandibular injury in the depletion of antioxidant protection at the systemic level and requires the development of pathogenetically substantiated correction means..
Conclusions. A fracture of the mandible deepens the severity of systemic disorders caused by acute blood loss and ischemia-reperfusion of the limb, one of the manifestations of which is a significantly greater depletion of the enzyme link of antioxidant protection in the liver after 1 and 7 days, which does not reach the control level by 14 days.
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