DEVELOPMENT AND EXPERIMENTAL REPLICATION OF THE MODEL OF PARTIAL TRACHEAL STENOSIS IN YOUNG SEXUALLY IMMATURE WHITE RATS

Abstract

This work is devoted to the development of two models of experimental replication of stenosis in the upper part of the trachea with different degrees of compression of this organ in sexually immature (one-month-old) white Wistar rats. Considering the different degrees of laryngomalacia in newborns, we developed two models: with a lower (20%) and higher (30%) degree of airway obstruction. In the first version of modeling, this was achieved by applying the ligature at the level between 1 and 2, or 2 and 3 cartilaginous semi-rings of the trachea, in the second – by applying it directly to the 2 cartilaginous semi-ring of the trachea. Both models were performed to study the state of the organism in conditions of hypoxic hypoxia in laboratory animals. The developed modeling methods differ from each other not only in the place of application of the compressing ligature, but also in the mechanism of compression development. In the case of applying a ligature to the intercartilaginous ligaments (20% stenosis), soft tissues are compressed and both semi-rings of the trachea are brought together. In the second variant of modeling, the pathophysiological mechanism of stenosis consists not only in the compression of the cartilaginous semi-ring of the trachea, but also in the process of invagination of the dorsal, i.e., elastic part of the trachea into the lumen of this hollow organ. As a result, a more intense variant of tracheal stenosis in experimental animals is achieved. Another important component of the developed models is the possibility at different stages of the experiment to eliminate the compressive effect of the ligature on the trachea and to study the state of various organs and tissues of animals in the early or delayed post-hypoxic periods. This leads to a significant increase in the value or efficiency of conducting this kind of experiments, taking into account the fact that hypoxic and posthypoxic periods can be studied on the same experimental animal. Both exotracheal modeling methods are fundamentally different from the endotracheal variant of experimentally reproducing stenosis. With the latter, pathological structural and functional disorders of the cells of the mucous membrane, the connective apparatus of the trachea and smooth muscle elements, the development of inflammation, and the progression of irreversible changes in the cellular and organ structures of the trachea are observed. In addition, simulation of the specified variant of stenosis requires the use of expensive equipment – a laryngoscope and some other modern technologies. Both variants of exotracheal modeling of tracheal stenosis, proposed by us, are devoid of all these shortcomings. At the same time, they enable to achieve the same degree of stenosis of this organ in animals as with the endotracheal variant.