PATHOGENETIC MECHANISMS OF THE DEVELOPMENT OF MORPHOLOGICAL CHANGES IN THE SKIN OF RATS IN THE MODELLING OF A THERMAL BURN

Abstract

Aim. The study was designed to perform a complex examination of the dynamics of the activity of protease inhibitor system along with the morphological study of cell and tissue components of the skin regeneration in the modelling of the 2nd degree thermal burn in rats.Materials and methods. The studies were conducted on 40 mature male Wistar rats. We determined the trypsin-like, elastase-like, antitrypsin activity and acid-stable inhibitors of proteinases in supernatants of homogenates of the skin of rats after the modelling of a burn injury by the enzymatic methods. The wound healing process was evaluated based on the macroscopic, histological examination with the general staining by hematoxylin and eosin, van Gieson’s picrofuchsin, and transmission electron microscopy.Results. The complex analysis of the skin regeneration revealed the role of the enzymatic reactions and the inflammatory microenvironment in the development of pathogenetic and morphological tissue changes in the dynamics of wound healing. The homeostasis of proteinase-inhibitory system was accompanied by both local and systemic disorders. The nonspecific proteinases occupied the key positions among the mediators of the biochemical alteration. The dynamics of changes was characterized by a powerful proteolysis with a progressive depletion of the inhibitory potential, which caused the development of a secondary-alterative process. The launch of the cascade of the inflammatory responses led to the disruption of the microcirculation and the damage of the blood-tissue barriers, the proteolytic destruction of the connective fibers, the formation of an edema and the disruption of the regenerative capacity of a damaged tissue. Morphological destructive changes in the skin remained up to 7-14 days, a decreased regenerative ability of the skin was manifested by a violation of the proliferation and differentiation of the epidermis. According to the electron microscopy, the phenomenon of tissue and intracellular edema, lesions of the microcirculatory bed, leukocyte-macrophage infiltration persisted up to 14 days of the experiment. The disruptions of the structure of the intercellular contacts between epidermocytes, macrophages in the dermis and many newly formed collagen fibers were still noticeable by the 14th day. Conclusion. The results of the study showed the progressive development of the destructive reactions after the modelling of 2nd degree thermal burn. There was an increase in the level of proteolytic activity on the background of depletion of the inhibitory potential. There was the persistence of the alterative changes in the skin up to 7-14 days and the complication of the reparative processes with suppuration, impaired proliferation and differentiation of the epidermis. The performed investigation is important for the determination of further ways of pathogenetic correction.