THE INFLUENCE OF ACUTE BLOODLOSS ON THE INTENSITY OF LIPID PEROXIDATION PROCESSES IN THE LIVER UNDER CONDITIONS OF CRANIO-CEREBRAL TRAUMA, BLUNT ABDOMINAL TRAUMA AND SKELETAL TRAUMA IN THE EXPERIMENT

Abstract

Introduction. Traumatism is one of the most pressing problems of our time and ranks the third place among the leading causes of death. In half of the cases, mortality from traumas is caused by acute blood loss. After a significant blood loss, the preconditions occur for the formation of active oxygen forms with increased free radical oxidation. In the context of modern trauma, acute blood loss is in most cases combined with mechanical injuries of various localizations. However, the influence of acute blood loss on the course of such injuries has not been sufficiently studied.

The aim of the study – to determine the influence of acute blood loss on the intensity of lipid peroxidation processes in the liver under conditions of cranio-cerebral trauma (CCT), blunt abdominal trauma (BAT), and ske­letal trauma (ST) in the experiment.

Research methods. In the experiments, 316 mature white male Wistar line rats weighing 200–220 g were used. All rats were divided into seven groups: control and six experimental groups. In the experimental groups, under thiopental-sodium anesthesia at a dose of 40 mg­·kg^-1, CCT, BAT, and ST were modeled, which were standar­di­zed by the amount of lethality. In separate groups of rats with mechanical injuries of various localizations, acute blood loss of 1,5 % of body weight was additionally modeled by transection of the femoral vein. After 3, 7, 14, 21 and 28 days of the posttraumatic period under anesthesia, rats of each experimental group were taken out of the experiment. The content of reagents to thiobarbituric acid (TBA-active LPO products) was determined in the liver homogenate extract.

Results and Discussion.  The modeled mechanical traumas of different localization of injury in the posttraumatic period initiate an increase in lipid peroxidation processes in the liver from the 3rd day of the posttraumatic period. The content of TBA-active lipid peroxidation products subsequently increases and decreases by the 28^th day, but only in the background of ST at this time the index reaches the control level. Additional blood loss in the context of modeled injuries significantly increases the intensity of lipid peroxidation in the liver. At all studied times of the post-traumatic period, the content of TBA-active products was statistically significantly higher than in rats with isolated trauma. Under these conditions, a single-phase increase was observed with a maximum after 7–14 days and a subsequent decrease by the 28^th day of the experiment. By the intensity of the increase in liver lipid peroxidation on the background of additional blood loss, the injuries were divided as follows: ST←CCT←BAT. The detected disorders should be taken into account during the development of systemic correction in conditions of skeletal trauma complicated by acute blood loss.

Conclusions. Acute blood loss significantly exacerbates the severity of systemic disorders under conditions of mechanical trauma of various localizations and contributes to an increase in the intensity of lipid peroxidation in the liver, the maximum of which occurs after 7–14 days of experiment with subsequent slow recovery up to the 28^th day, which does not reach the control level.