DYNAMICS OF PATHOMORPHOLOGICAL CHANGES OF THE MYOCARDIUM IN CHRONIC EXPERIMENTAL ENDOTOXICOSIS

Abstract

Relevance. Modeling the conditions of endotoxicosis by introducing bacterial lipopolysaccharide against the background of toxic liver damage is due to the fact that under such conditions the situation that accompanies almost every chronic pathology, including cardiovascular, is reproduced. The release of substances that play a role in the formation of endogenous intoxication causes heart damage in the absence of cardiac pathology, and in its presence worsens the course and prognosis. However, it should be found out whether these changes are the result of only toxic damage to cardiomyocytes or have another morphological basis and what their dynamics are.
 Objective: to characterize the morphological changes of the myocardium in experimental chronic endotoxicosis.
 Materials and methods. The research was carried out by modeling endotoxicosis in 18 laboratory animals for 90 days by daily intragastric injection of tetrachloromethane at the rate of 3-5 ml/kg of body weight and every 6th day by intraperitoneally adding bacterial lipopolysaccharide at a dose of 0.2 mg/kg of body weight. Animals were removed from the experiment by decapitation at 30, 60, and 90 days. Animals were removed from the experiment by decapitation after anesthesia with intraperitoneal administration of sodium thiopental at a dose of 50 mg/kg. The control group consisted of 6 intact animals. For histological examination, myocardial tissue was condensed in paraffin, and deparaffinized sections were stained with hematoxylin and eosin, examined for the detection of neutral glycosaminoglycans and acidic mucopolysaccharides, stained with Alcian blue and PAS-reaction according to standard methods, and examined under a Nikon Eclipse Ci-E light microscope.
 Results. During researching the myocardium at the light-optical level of experimental animals, after 30 days of chronic endogenous intoxication caused by injection of tetrachloromethane and bacterial LPS, it undergoes changes, first of all, it concerned cardiomyocytes: we observe thinned cells around the vessels and unchanged ones at a distance from the vessels. In some of them, hyperchromia of the nuclei and phenomena of contractile damage and fiber fragmentation were noted. Manifestations from the CMC increased during the next period of the experiment: after 60 days, expressed wave-like deformation of fibers with atrophic changes in muscle cells was detected in the myocardium. Hemodynamic changes were characterized by hyperemia, the number of perivascular hemorrhages increased. On the 90th day of the experiment, in addition to inflammatory manifestations and dystrophic-necrotic changes, cardiomyocyte atrophy in combination with expressed interstitial edema was detected in the myocardial tissue of animals. In the stroma, in addition to small foci of perivascular cardiosclerosis, foci of adipocyte growth were determined. Cardiomyocyte defibrillation and hemorrhages were observed in some areas
 Conclusion. The intensity of structural changes in cardiomyocytes and hemodynamic disorders in chronic endotoxicosis depends on the duration of intoxication and the character of structural changes. The interstitium of the myocardium of rats under experimental endotoxicosis conditions is dystrophic-sclerotic and is manifested by a different combination of edematous and sclerotic manifestations at different stages of exposure to toxicants.