STRUCTURAL REACTION OF PULMONARY TISSUE AND BLOOD VESSELS OF SMALL CIRCLE OF BLOOD CIRCULATION IN THE TERMINAL STAGE OF ACUTE PERITONITIS

Abstract

The aim of our investigation was an experimental study of changes in the structure of pulmonary tissue and vessels of the pulmonary circulation at the terminal stage of acute peritonitis.

Materials and Methods. Morphometric (measurement of thickness of interalveolar septa and diameter of alveoli) histological for the studying the structure of lung tissue and vessels with light-optical microscopy, statistical. The experiments were performed on 40 white male rats: 10 animals made up an intact control group; acute peritonitis (terminal stage) was modeled in 30 animals.

Results and Discussion. The character and dynamics of structural changes development, the range of compensatory and adaptive reactions are the fundamental component of the searching for correction of the negative impact of pathological factors to the body. The study of peritonitis remains an urgent problem of modern clinical medicine. Since peritonitis leads to severe organ pathology, the development of multiple organ failure and death. Further narrowing of the lumen of the alveoli and accumulation of the transudate in the pulmonary interstitium were found after 36 hours from the start of the experiment. In the terminal phase, a paralyzed expansion of the arterial lumen and a collapsed state of the veins were observed. The character of the morpho-functional changes in the lung tissue and vessels of the small circulation, established in the process of experiment, their dynamics and depth testify to the pronounced effect of toxic metabolic products in the development of endotoxicosis.

Conclusions. Experimental acute peritonitis in white male rats at the terminal stage caused a significant narrowing of the diameter of the alveoli and the lumen of bronchioles against the background of a significant thickening of the interalveolar septa. Endotoxicosis in the conditions of this pathology caused the development of dystrophic processes and disruption of normal tissue-vascular relationships in the lung tissue.