ABSTRACT
Ventilator-induced lung injury (VILI) is associated to a high rate of mortality with an important social impact. Mechanical ventilation induces structural and ultrastructural alterations in all cell types of the lung and can derive in the transduction of intracellular signals, as well as in changes in the expression of genes, a process known as mechanotransduction. Some of the conditions involved, such as inflammation and/or coagulation, apoptosis/necrosis can lead to the propagation of the injury outside the lung, resulting in multiorganic failure. VILI can be modulated by means of diverse interventions as the use of protective ventilatory modes, therapeutic approaches based on vasoactive and antioxidative drugs, and more recently treatments based on the use of repairing substances of the surfactant like poloxamers among others. Knowledge of the mechanisms involved in VILI is definitive for a better approach to this condition.
Subject(s)
Respiration, Artificial/adverse effects , Respiratory Distress Syndrome/etiology , Animals , Antioxidants/therapeutic use , Biophysical Phenomena , Biophysics , Calcium/metabolism , Capillary Fragility , Capillary Leak Syndrome/etiology , Cell Membrane/ultrastructure , Cytokines/antagonists & inhibitors , Cytokines/metabolism , Cytoskeleton/ultrastructure , Elasticity , Epoprostenol/therapeutic use , Humans , Lung/blood supply , Lung/pathology , Models, Biological , Multiple Organ Failure/etiology , Positive-Pressure Respiration , Pulmonary Edema/etiology , Rabbits , Respiratory Distress Syndrome/metabolism , Respiratory Distress Syndrome/pathology , Respiratory Distress Syndrome/physiopathology , Respiratory Distress Syndrome/prevention & control , Signal Transduction , Stress, MechanicalABSTRACT
La lesión pulmonar inducida por la ventilación mecánica (VILI) se asocia a una elevada tasa de mortalidad y a un importante impacto social. La ventilación mecánica induce alteraciones estructurales y ultraestructurales en todas las tipologías celulares que conforman el pulmón, que pueden derivar en la transducción de señales intracelulares, así como en cambios en la expresión de genes, en lo que se conoce como mecanotransducción. Entre los procesos implicados están la inflamación y/o coagulación, apoptosis/necrosis que pueden derivar en la propagación de la lesión fuera del pulmón, llegando a la afectación multiorgánica. La VILI puede ser modulada mediante intervenciones diversas como el uso de modalidades ventilatorias protectoras, abordajes terapéuticos basados en fármacos vasoactivos, antioxidantes, y más recientemente tratamientos basados en el uso de sustancias reparadoras del surfactante como los poloxámeros entre otros. El conocimiento de los mecanismos implicados en la VILI es definitivo para el abordaje de esta patología
Ventilator-induced lung injury (VILI) is associated to a high rate of mortality with an important social impact. Mechanical ventilation induces structural and ultrastructural alterations in all cell types of the lung and can derive in the transduction of intracellular signals, as well as in changes in the expression of genes, a process known as mechanotransduction. Some of the conditions involved, such as inflammation and/or coagulation, apoptosis/necrosis can lead to the propagation of the injury outside the lung, resulting in multiorganic failure. VILI can be modulated by means of diverse interventions as the use of protective ventilatory modes, therapeutic approaches based on vasoactive and antioxidative drugs, and more recently treatments based on the use of repairing substances of the surfactant like poloxamers among others. Knowledge of the mechanisms involved in VILI is definitive for a better approach to this condition
Subject(s)
Humans , Respiratory Distress Syndrome/etiology , Respiration, Artificial/adverse effects , Respiratory Distress Syndrome/physiopathology , Stress, Mechanical , Inflammation Mediators/therapeutic use , Pulmonary Surfactants/therapeutic useABSTRACT
The release of endogenous glucocorticoids is critical in regulating the severity of disease activity in patients with inflammatory conditions such as rheumatoid arthritis (RA). Blocking cortisol production results in a flare-up in disease activity in RA patients, and surgical removal of the adrenals in patients with Cushing's disease has been reported to exacerbate autoimmune disease. In adjuvant-induced arthritis (AA; a rat model of RA), there is an activation of the hypothalamo-pituitary-adrenal (HPA) axis associated with the development of inflammation. In addition, there are profound changes in peptides within the paraventricular nucleus, which are responsible for regulating the HPA axis. These changes have profound implications on the ability of AA rats to respond to acute stress. Understanding the regulation of the HPA axis in health and disease holds out the promise of targeted therapy to alleviate inflammatory conditions. This article will consider the impact of stress on an individual and his or her susceptibility to inflammation. We wish to question the idea that stress is "all bad." As we shall see, exposure to a single acute stressor can alter the phenotype of the rat to change it from being susceptible to resistant in autoimmune disease models. This alteration in susceptibility takes days to manifest itself, but can last for weeks, suggesting beneficial effects of exposure to an acute stressor.
