Abstract:
Despite the fact that the main pathogenetic factor in the development of burn disease is
the alteration of the skin, the severity of the condition of patients in the acute period of
the disease is due to systemic changes in the body caused by thermal factor. Being a
powerful stress factor, severe burns are accompanied by activation of the hypothalamicpituitary
system. Although thyroid hormones are not considered typical "stress
hormones", they also play a role in maintaining vasomotor function under stress. The
question of thyroid dysfunction on the background of burn injury remains debatable,
and scientific data on its morphological and ultramicroscopic changes are quite limited.
The aim of the work is to establish microscopic and submicroscopic changes of the
thyroid gland of experimental animals in the stage of shock after thermal trauma of the
skin. Experimental studies were performed on 12 white adult male rats, which received
a thermal burn of the skin of 2-3 degrees with a lesion area of 21-23 % of the skin. An
infusion of 0.9 % NaCl solution at a dose of 10 ml/kg was performed into the inferior
vena cava. Collection of material for histological and electron microscopic examinations
was performed according to generally accepted methods. Histological specimens were
examined using a MIKROmed SEO SCAN light microscope and photo-documented
using a Vision CCD Camera with an image output system from histological specimens.
Ultrathin sections made on an ultramicrotome UMPT-7 were contrasted with uranyl
acetate, lead citrate according to the Reynolds method and studied under an electron
microscope PEM-125K. Conducted micro- and submicroscopic studies of the structural
components of the thyroid gland a day after the reproduction of thermal trauma to the
skin on the background of the introduction of 0.9 % NaCl solution revealed reactive
adjunctive-compensatory changes and initial manifestations of destruction. Vascular,
stromal and parenchymal components of the organ in the stage of shock after burns
correspond to the state of "stress" as a reaction to pathological exogenous exposure,
and the intensification of metabolic processes in the affected organism of experimental
animals.
