Гістологічні зміни компонентів аерогематичного бар’єру через 24 години після моделювання гострої ниркової недостатності

Abstract

Nowadays, acute renal failure remains one of the most complex problems in modern medicine. Multiple studies have proved that acute renal failure is frequently accompanied by the development of acute lung injury and its most severe form – acute respiratory distress syndrome. According to the literature, lethality in case of acute lung injury or acute respiratory distress syndrome is extremely high and is 30-65%. In case of combination of acute renal failure and acute lung injury or acute respiratory distress syndrome, the most frequently observed in critical patients, lethality reaches 80%. The purpose of the study was to study the possibility of ultrastructural changes of the respiratory tract in the lungs due to experimental modeling of acute renal failure. Materials and methods. The experiments were performed on 30 mature white male rats weighting 180-220 grams. Acute renal failure was induced by intramuscular administration of 50% glycerol water solution in dose of 10 ml per 1 kg of body mass. The sampling of lung tissue for electron microscopy study was carried out under the ketamine anaesthesia in 24 hours after beginning of the experiment. The pieces of lung tissue were fixed in 2.5% solution of gluteraldehyde with further postfixation in 1% solution of osmium tetroxide. After dehydration, the material was poured over epon araldite. The cuts, obtained on ultramicrotome “Tesla BS-490”, were studied using electron microscope “PEM-125K”. Results and discussion. In 24 hours after the beginning of the experiment, the changes in the alveolocytes of types I and II, endotheliocytes, alveolar macrophages are accompanied by the development of intracellular edema with ultrastructural disorder of organelles. Because of endotheliocytes edema and aggregation of forming blood elements, some blood capillaries lumens are closed or drastically narrowed. In some blood capillaries, we observe disorder of the luminal membrane integrity of endothelial cells accompanied by exit of the intracellular content into the micro blood vessel lumen. The expressed disorders of structural organization of the components of pulmonary aero-hematic barrier cause the exit of forming blood elements into the interstitial tissue and alveoli. Conclusion. Тhe detected changes in 24 hours of the experiment have a dystrophic-destructive character and are manifested by the development of edema in alveolocytes of types I and II, alveolar macrophages, endotheliocytes of hemocapillaries. Perspective for further research. Considering the severity of ultrastructural changes that develop in experimental acute renal failure, it would be reasonable to conduct a further study in order to find possible methods of prevention and timely correction