Abstract
Acute respiratory distress syndrome (ARDS) is a common complication of many diseases. Its polyetiological pattern determines the specific features of lung morphological changes and the clinical course of ARDS. Objective: to analyze the pathogenesis of ARDS in the context of the general pathological processes underlying its development. Material and methods. More than 200 lungs from the people who had died from severe concomitant injury or ARDS-complicated pneumonia were investigated. More than 150 rat experiments simulated various types of lung injury: ventilator-induced lung injury with different ventilation parameters; reperfusion injuries (systemic circulation blockade due to 12-minute vascular fascicle ligation, followed by the recovery of cardiac performance and breathing); microcirculatory disorder (injection of a thromboplastin solution into the jugular vein); blood loss; betaine-pepsin aspiration; and closed chest injury. Different parts of the right and left lungs were histologically examined 1 and 3 hours and 1 and 3 days after initiation of the experiment. Lung pieces were fixed in 10% neutral formalin solution and embedded in paraffin. Histological sections were stained with hematoxylin and eosin and using the van Gieson and Weigert procedures; the Schiff test was used. Results. The influence of aggression factors (trauma, blood loss, aspiration, infection, etc.) results in damage to the lung and particularly air-blood barrier structures (endothelium, alveolar epithelium, their basement membrane). In turn the alteration of cellular and extracellular structures is followed by the increased permeability of hemomicrocirculatory bed vessels, leading to the development of non-cardiogenic (interstitial, alveolar) pulmonary edema that is a central component in the pathogenesis of ARDS. Conclusion. The diagnosis of the early manifestations of ARDS must account for the nature of an aggression factor, the signs confirming the alteration of the lung and particularly air-blood barrier structures, pulmonary oxygenizing dysfunction, the development of noncardiogenic pulmonary edema; the absence of left ventricular failure signs. Key words: acute respiratory distress syndrome, pathogenesis.
Highlights
Острый респираторный дистресс синдром (ОРДС) является частым осложнением многих заболеваний
Its polyetiological pat tern determines the specific features of lung morphological changes and the clinical course of Acute respiratory distress syndrome (ARDS)
More than 200 lungs from the people who had died from severe concomitant injury or ARDS complicated pneumonia were investigated
Summary
Диагностика ранних про явлений ОРДС должна учитывать характер фактора агрессии, признаки, подтверждающие альтерацию легких, и, в ча стности, структур аэрогематического барьера. The influence of aggression factors (trauma, blood loss, aspiration, infection, etc.) results in damage to the lung and air blood barrier structures (endothelium, alveolar epithelium, their basement membrane). The diagnosis of the early manifestations of ARDS must account for the nature of an aggres sion factor, the signs confirming the alteration of the lung and air blood barrier structures, pulmonary oxygenizing dysfunction, the development of noncardiogenic pulmonary edema; the absence of left ventricular fail ure signs. Острый респираторный дистресс синдром (ОРДС) является одной из важнейших проблем анестезиологии реаниматологии. Это и определило целесообразность и направление наших исследований.В данном исследовании рассмо трены основные звенья патогенеза ОРДС, касающие ся ранних признаков повреждения легких, развития некардиогенного отека легких, нарушений микро циркуляции в легких, клеточной реакции, обуслов ленной привлечением в легкие иммунокомпетентных клеток. Неговского РАМН [2,3,4,5,6,7,8,9]
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.