Structural changes of lung tissues in the dynamics of inhalation poisoning with carbonic acid dichlorohydride

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Abstract

A study of structural changes in lung tissue during the formation of organ edema due to inhalation of a lipotropic poison, carbonic acid dichloride, showed the peculiarities of the formation of acute respiratory distress syndrome. The point of application of the poison is the distal bronchioles, the epithelium of which is subject to dystrophic and necrotic changes followed by goblet metaplasia. The absorbed poison causes pronounced changes in blood microcirculation, steroid-resistant NO-mediated endothelial dysfunction with blood deposition in dilated capillaries, aggregation and lysis of erythrocytes. Changes in the vascular bed in the interalveolar septa precede the formation of an acute inflammatory reaction with the accumulation of alveolar effusion and dystrophic changes in the alveolar epithelium with cell desquamation. Among the cells of the alveolar lining, type II alveolocytes are the most vulnerable. Plasma permeation of the connective tissue of the interalveolar septa interstitium is accompanied by their infiltration with polymorphonuclear leukocytes and activation of macrophages. Desquamation of epithelial cells of the distal bronchioles leads to obstruction of their lumens and, through the valve mechanism, contributes to overextension of the alveoli with the formation of emphysema and reduction of capillary blood circulation in the alveolar septa. The observed changes determined the directions for improving the treatment of poisoning by asphyxiating poisons.

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P. A. Torkunov

Kirov Military Medical Academy

Author for correspondence.
Email: tpa4@mail.ru
Russian Federation, St. Petersburg

S. V. Chepur

State Research Testing Institute of Military Medicine

Email: tpa4@mail.ru
Russian Federation, St. Petersburg

P. D. Shabanov

Kirov Military Medical Academy

Email: tpa4@mail.ru
Russian Federation, St. Petersburg

A. V. Zemlyanoy

Scientific Research Institute of Hygiene, Occupational Pathology and Human Ecology

Email: tpa4@mail.ru
Russian Federation, Kuzmolovsky settlement, Leningrad Region

O. V. Torkunova

State Pediatric Medical University

Email: tpa4@mail.ru
Russian Federation, St. Petersburg

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2. Fig. 1. The structure of the lung parenchyma in mice 30 min after inhalation exposure to carbonic acid dichloride at a dose of 1 LCt50. Hematoxylin and eosin staining. (a) - plethora of capillaries of the septa prolapsing into the lumen of the alveoli (object ×20); (b) - plethora of venous vessels with swelling of the septa and oozing of protein-containing fluid into the lumen of the alveoli (object ×40); (c) - staged changes in the respiratory alveolocyte due to the colloid-osmotic state of the cytosol and underlying connective tissue; (d) - changes in membrane-bound and luminal cells of the alveolar epithelium and macrophages (object ×100); (d) - karyorrhexis in endothelial cells and infiltration of the septum by polymorphonuclear leukocytes involved in the resorption of alveolar effusion (object ×100).

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3. Fig. 2. The structure of the lung parenchyma in mice 3 hours after inhalation exposure to carbonic acid dichloride at a dose of 1 LCt50. Hematoxylin and eosin staining. (a) - diagram of the developing histopathological changes (explanations in the text); (b) - plasmalemmal septal venules (object ×40); (c) - expansion of the alveolar lumens with resorbable protein effusion with plethora of partially thrombosed septal vessels (object ×20); (d) - dystrophic changes in the bronchial epithelium with apical necrosis, with rejection of a part of the cell cytosol and death of alveolocytes as part of the epithelial layer (object ×100); (d) — infiltration of the interalveolar septa by polymorphonuclear leukocytes (object ×100); (e) — microthrombi in the capillaries of the septa and foci of erythrocyte diapedesis into the lumen of the alveoli (object ×40).

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4. Fig. 3. The structure of the lung parenchyma in mice 1 day after inhalation exposure to carbonic acid dichloride at a dose of 1 LCt50. Hematoxylin and eosin staining. (a) — diagram of developing histopathological changes (explanation in the text); (b) — metaphase “plates” in the surviving alveolocytes of the acinar ducts (object ×100); (c) — dystonic expansion of septal vessels, accompanied by dystrophic changes in the cells of the muscular layer of the vessel and plasma impregnation of the paravasal connective tissue (object ×40); (d) — dystrophic changes in cells and desquamation of the epithelium into the lumen of the alveoli with resorption of effusion by activated forms of macrophages (object ×100); (d) — emphysema of alveoli free of effusion, in the overstretched septa of which a reduction of capillaries with small aggregates of lysed erythrocytes was observed (object ×20); (e) — dystrophic changes and death of bronchial epithelial cells with the accumulation of cellular detritus seeded with coccal flora in the lumen (object ×100).

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