Structural characteristics of the lungs in experimental inertial traumatic brain injury and endotoxinemia

Aim. To investigate the morphological characteristics of the lungs in experimental closed inertial traumatic brain injury (TBI) and endotoxinemia. Materials and methods. Inertial TBI was reproduced using a setup in which a 200 g load was dropped from a height of 1 m onto the parietal region of the rat head. Endotoxinemia was simulated by repeated intramuscular injections of pyrogenal solution. The animals were divided into the following groups: (1) intact rats ( n = 12); (2) animals after TBI ( n = 12); (3) triple injection of pyrogenal without TBI ( n = 12); and (4) triple injection of pyrogenal immediately after TBI ( n = 12). On day 6 from the onset of the experiment, the lungs were removed and histochemically detected for calcium cations using alizarin red C and boric acid staining or the Von Kossa method. Argyrophilic fiber was determined using Foot’s method. The status of mast cells was assessed using toluide blue. Immunohistochemistry was used to detect the expression of the CD14 receptor and endothelin 1. The lung tissue was subjected to morphometric analysis. Results. In the lungs of animals with simulated endotoxemia, a significant increase in the thickness of the interalveolar septa and adventitial cuffs of the distal branches of the pulmonary arteries was observed. The thickness of the internal and external elastic membranes of the bronchial arteries, as well as the argyrophilicity of connective tissue fibers, alveoli, and distal fourth-order airways, also increased. A decrease in the spectral fluorescence intensity of elastic fibers in connective tissue near vessels and bronchi was observed, as well as a decrease in the thickness of the adventitia of the caudal pulmonary veins and the lumen diameter of the third- and fourthorder intrapulmonary bronchi. Increased levels of endothelin-1, CD14-positive, and mast cells were observed in the perivascular space and bronchial lumen. Conclusion. The results obtained demonstrate that endotoxinemia in the acute phase of TBI initiates morphofunctional signs of systemic inflammation in the lungs.