Mechanical ventilation with moderate tidal volumes synergistically increases lung cytokine response to systemic endotoxin

Altemeier, William A.; Matute-Bello, Gustavo; Frevert, Charles W.; Kawata, Yasunobu; Kajikawa, Osamu; Martin, Thomas R.; Glenny, Robb W.

doi:10.1152/ajplung.00004.2004

Cited by 149 publications

(158 citation statements)

References 39 publications

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“…Numerous experimental models of VILI have demonstrated additive or synergistic effects of bacterial products with mechanical ventilation on the development or exacerbation of lung injury [44][45][46][47][48]. Mechanical ventilation using moderate tidal volumes in mice enhanced lipopolysaccharide (LPS)-induced expression of TNF-α, IL-8, growth-related protein-α and monocyte chemoattractant protein (MCP)-1 [44].…”

Section: Epithelial Cell Responses To Mechanical Stretchmentioning

confidence: 99%

Role of the pulmonary epithelium and inflammatory signals in acute lung injury

Manicone¹

2009

Expert Review of Clinical Immunology

118

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Acute lung injury (ALI) is a clinical disease marked by respiratory failure due to disruption of the epithelial and endothelial barrier, flooding of the alveolar compartment with protein-rich fluid and recruitment of neutrophils into the alveolar space. ALI affects approximately 200,000 patients annually in the USA and results in approximately 75,000 deaths. It is associated with prolonged mechanical ventilation, intensive medical care, high morbidity and mortality, and rising healthcare costs. Owing to its impact on public health, great strides have been made towards understanding the pathobiology of ALI to affect outcome. This review will focus on the role of the epithelial cell in the pathogenesis and resolution of ALI and the role of various inflammatory mediators in ALI. Keywordsβ2-agonist; acute lung injury; acute respiratory distress syndrome; chemokine; cytokine; epithelial cell; inflammation; methylprednisolone; neutrophil; salbutamol; steroid; ventilator-induced lung injuryAcute lung injury/acute respiratory distress syndrome (ALI/ARDS) was first described in 1967 by Ashbaugh and colleagues in a group of 12 patients who shared a constellation of clinical symptoms including acute respiratory distress, hypoxemia refractory to supplemental oxygen, decreased lung compliance and diffuse pulmonary infiltrates [1]. Since this first description, the clinical criteria have evolved to include acute onset of respiratory distress, bilateral pulmonary infiltrates seen on chest radiographs, absence of left-sided heart failure and hypoxemia, with the severity of hypoxemia distinguishing ALI and ARDS (Box 1) [2]. Extrapolating from recent epidemiologic studies using these criteria, ALI affects about 200,000 patients annually in the USA and results in approximately 75,000 deaths [3]. This disease, which can be caused by common events such as pneumonia, sepsis and trauma, results in high morbidity, mortality and healthcare expenditures associated with prolonged mechanical ventilation and intensive care. Because of its impact on public health and patient outcomes, great strides have been made towards understanding the pathobiology of ALI.When defined broadly to include all processes related to defense against microbes, other environmental insults and injury, a wide variety of cell types and proteins participate in inflammation and immunity. Leukocytes are the paradigmatic inflammatory cell type, but they are not the only cells that function in defense and immunity. The epithelial lining of all tissues forms a continuous barrier to the environment and is the first line of defense against infectious agents and toxins. Though specialized to serve distinct functions among tissues, epithelial cells respond similarly to injury and infection, and regulate leukocyte influx through the production of proinflammatory cytokines, chemokines and other factors that modulate chemokine gradients and effect leukocyte migration. This review will focus on the role of the pulmonary epithelium and inflammatory mediators in ALI. More s...

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Section: Epithelial Cell Responses To Mechanical Stretchmentioning

confidence: 99%

Role of the pulmonary epithelium and inflammatory signals in acute lung injury

Manicone¹

2009

Expert Review of Clinical Immunology

118

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“…Large tidal volumes (V T ) contribute to and worsen the acute respiratory distress syndrome (ARDS) in Intensive Care Unit (ICU) patients after hours or days of ventilation [1][2][3][4][5][6][7][8] . Recent studies suggest intraoperative ventilation settings affect postoperative pulmonary outcomes 1,[9][10][11][12][13] .…”

Section: Introductionmentioning

confidence: 99%

Early Effect of Tidal Volume on Lung Injury Biomarkers in Surgical Patients With Healthy Lungs

Fernandez-Bustamante

Klawitter

Repine

et al. 2015

Survey of Anesthesiology

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“…In addition to being temporally progressive, (21) this cytokine synthesis is potentiated by concomitant factors, such as systemic endotoxins and hyperoxia. (22,23) …”

Section: From Volutrauma To Biotraumamentioning

confidence: 99%

“…In addition to being temporally progressive, (21) this cytokine synthesis is potentiated by concomitant factors, such as systemic endotoxins and hyperoxia. (22,23) Based on the induction of a proinflammatory response in the lung epithelium associated with an alteration in permeability in the local endothelium, (14,24) some authors have suggested that there is decompartmentalization of…”

Section: From Volutrauma To Biotraumamentioning

confidence: 99%

Citoesqueleto e mecanotransdução na fisiopatologia da lesão pulmonar induzida por ventilador

Taniguchi¹,

Caldini

Velasco

et al. 2010

J. bras. pneumol.

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Although mechanical ventilation is an important therapy, it can result in complications. One major complication is ventilator-induced lung injury, which is caused by alveolar hyperdistension, leading to an inflammatory process, with neutrophilic infiltration, hyaline membrane formation, fibrogenesis and impaired gas exchange. In this process, cellular mechanotransduction of the overstretching stimulus is mediated by means of the cytoskeleton and its cell-cell and cell-extracellular matrix interactions, in such a way that the mechanical stimulus of ventilation is translated into an intracellular biochemical signal, inducing endothelial activation, pulmonary vascular permeability, leukocyte chemotaxis, cytokine production and, possibly, distal organ failure. Clinical studies have shown the relationship between pulmonary distension and mortality in patients with ventilator-induced lung injury. However, although the cytoskeleton plays a fundamental role in the pathogenesis of ventilator-induced lung injury, there have been few in vivo studies of alterations in the cytoskeleton and in cytoskeleton-associated proteins during this pathological process.Keywords: Respiration, artificial; Cytoskeleton; Cell adhesion molecules; Focal adhesions; Mechanotransduction, cellular. ResumoA ventilação mecânica é uma terapia importante, mas pode resultar em complicações. Uma das mais relevantes é a lesão pulmonar induzida por ventilador. Devido à hiperdistensão alveolar, o pulmão inicia um processo inflamatório, com infiltrado neutrofílico, formação de membrana hialina, fibrogênese e prejuízo de troca gasosa. Nesse processo, a mecanotransdução da hiperdistensão celular é mediada através do citoesqueleto da célula e de suas interações com a matriz extracelular e com as células vizinhas, de modo que o estímulo mecânico da ventilação se traduz em sinalização bioquímica intracelular, desencadeando ativação endotelial, permeabilidade vascular pulmonar, quimiotaxia leucocitária, produção de citocinas e, possivelmente, lesão de órgãos à distância. Estudos clínicos demonstram essa relação entre distensão pulmonar e mortalidade em pacientes com lesão pulmonar induzida por ventilador. Entretanto, apesar de o citoesqueleto ter um papel fundamental na patogênese da lesão pulmonar induzida por ventilador, a literatura carece de estudos utilizando modelos in vivo sobre as alterações do citoesqueleto e de suas proteínas associadas durante esse processo patológico. Subsequent studies focused on the mechanical factors that triggered VILI, such as peak inspiratory pressure and V T .(9-12) Dreyfuss et al. confirmed the findings of Webb and Tierney and demonstrated that V T was the major determinant of alveolar injury and alveolocapillary membrane injury, which gave rise to the term "volutrauma". (13,14) In an important study, they compared rats ventilated with high V T and negative pressure (through a negative pressure ventilator, known as iron lung) with rats ventilated with high pressure and low V T (with thoracoabdominal movement restricte...

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Mechanical ventilation with moderate tidal volumes synergistically increases lung cytokine response to systemic endotoxin

Cited by 149 publications

References 39 publications

Role of the pulmonary epithelium and inflammatory signals in acute lung injury

Role of the pulmonary epithelium and inflammatory signals in acute lung injury

Early Effect of Tidal Volume on Lung Injury Biomarkers in Surgical Patients With Healthy Lungs

Citoesqueleto e mecanotransdução na fisiopatologia da lesão pulmonar induzida por ventilador

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