THE PECULIARITIES OF FREE RADICAL OXIDATION AT THE EXPERIMENTAL CRUSH-SYNDROME DEVELOPMENT

Abstract

Introduction. Researchers are particularly interested in studying the features of free radical oxidation in the crush-syndrome because in the genesis of capillary permeability and edema disturbance during the development process, one of the most important mechanisms is to enhance of free radicals generation.

The aim of the study – to investigate in dynamics the indicators of free radical oxidation in the blood and liver of rats on the model of endotoxicosis, which is formed in the conditions of the crush-syndrome.

Research Methods. Experiments were conducted on 40 adult white male rats. The experimental model was a pathological process that developed in animals as a result of the compression of the soft tissues of the left pelvic limb for 4 hours in a special device. The area of the compressive surface was 4 cm², and the force of compression was 4.25 kg/cm². At the same time, the integrity of large vessels and bone structures of the lower limb was maintained. Thus, a moderate degree of crush-syndrome was simulated.

The content of lipid hydroperoxides and the concentration of TBA-active products were determined in serum and liver. The level of production of reactive oxygen species by blood leukocytes was determined cytofluorimetrically.

Results and Discussion. The results of the study indicate the activation of the processes of free radical oxidation in the serum and liver of rats in the development of crush-syndrome. A significant increase in reactive oxygen species production by leukocytes during all periods of observation was established, changes in the indices of primary and secondary peroxidation were established. Comparing changes in the concentration of primary lipid peroxidation products in the serum and the liver homogenate supernatant of rats with experimental crush-syndrome, unidirectional changes in the concentration of lipid hydroperoxides in the studied biological fluids were found with their prevalence in the liver for 3–14 days. Comparison of the concentration of TBA-active products in the blood and liver of rats in the dynamics of the development of crush-syndrome also indicates an unidirectional growth of the studied indicator for 3–7 days with a subsequent decrease on the 14th day. It should be noted that on the 3rd day the concentration of TBA-AP prevailed in the liver homogenate, whereas on the 14th day the level of this indicator was 16.9 % less in the liver, relative to the blood.

Conclusion. In case of experimental crush syndrome activation of free radical oxidation processes is characterized by an increase in reactive oxygen species production by blood leukocytes during all periods of observation, as well as significant changes in the indices of primary and secondary peroxidation in the blood and the liver homogenate compared with the control group.