The role of endocrine mechanisms in ventilator-associated lung injury in critically ill patients.
The critically ill subjects are represented by a heterogeneous group of patients suffering from a life-threatening event of different origin, e.g. trauma, cardiopulmonary failure, surgery or sepsis. The majority of these patients are dependent on the artificial lung ventilation, which means a life-saving chance for them. However, the artificial lung ventilation may trigger ventilation-associated lung injury (VALI). The mechanical ventilation at higher volumes (volutrauma) and pressure (barotrauma) can cause histological changes in the lungs including impairments in the gap and adherens junctions and desmosomes. The injured lung epithelium may lead to an impairment of the surfactant production and function, and this may not only contribute to the pathophysiology of VALI but also to acute respiratory distress syndrome. Other components of VALI are atelectrauma and toxic effects of the oxygen. Collectively, all these effects may result in a lung inflammation associated with a subsequent profibrotic changes, endothelial dysfunction, and activation of the local and systemic endocrine responses such as the renin-angiotensin system (RAS). The present review is aimed to describe some of the pathophysiologic aspects of VALI providing a basis for novel therapeutic strategies in the critically ill patients.
Laboratory of Human Endocrinology, Institute of Experimental Endocrinology, Slovak Academy of Sciences, Bratislava, Slovakia. adela.penesova@savba.sk
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Penesova
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Galusova
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Vigas
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Vlcek
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Imrich
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Majek
D000311:Adrenal Glands / Q000378:metabolism; D000818:Animals; D016638:Critical Illness; D004703:Endocrine System / Q000378:metabolism* / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000378:metabolism; D005938:Glucocorticoids / Q000378:metabolism; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D012084:Renin-Angiotensin System; D012121:Respiration, Artificial / Q000009:adverse effects*; D055397:Ventilator-Induced Lung Injury / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control
D005938:Glucocorticoids; D018836:Inflammation Mediators