Lower tidal volume ventilation and plasma cytokine markers of inflammation in patients with acute lung injury*

Parsons, Polly E.; Eisner, Mark D.; Thompson, B. Taylor; Matthay, Michael A.; Ancukiewicz, Marek; Bernard, Gordon R.; Wheeler, Arthur P.

doi:10.1097/01.ccm.0000149854.61192.dc

Cited by 642 publications

(499 citation statements)

References 36 publications

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“…Parsons and colleagues support the interpretation that inflammation and mechanical injury are pathophysio logically linked in the lungs, because a simple intervention, reducing tidal volume, reduced systemic inflammation and also improved outcome (35). Thus, a portion of the lung inflam matory response is likely to be a consequence of direct mechanical injury to the lung parenchyma and circulating cytokines are markers of this inflammatory response.…”

Section: Discussionmentioning

confidence: 96%

“…There is strong evidence that IL6, IL8 and IL10 are useful circulating markers of the intensity of the inflam matory response in the lungs and the prognosis of patients at the onset of lung injury (35). Parsons and colleagues support the interpretation that inflammation and mechanical injury are pathophysio logically linked in the lungs, because a simple intervention, reducing tidal volume, reduced systemic inflammation and also improved outcome (35).…”

Section: Discussionmentioning

confidence: 99%

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Thoracotomy procedures effect cytokine levels after thoracoabdominal esophagectomy

Frick

Justinger²,

Rubie³

et al. 2011

Oncol Rep

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Abstract. Pulmonary complications together with surgical complications are the most frequent causes for morbidity and mortality after thoracoabdominal esophagectomy. The con tinuous improvement of surgical techniques has led to a decrease in surgical complications, whereas up to 30% of the patients develop postoperative pulmonary complications such as acute lung injury (ALI) or even the more severe acute respiratory distress syndrome (ARDS), which are characterized by an acute inflammation in the lung parenchyma and the airspace. Evidence from several studies indicates that a complex network of inflammatory cytokines and mediators play a key role in mediation, amplification, and perpetuation of the process of lung injury and that the thoracotomy itself is a risk factor for developing ALI or ARDS. In this trial, the cytokine levels of IL6, IL8 and IL10 were measured and compared in 30 patients who had undergone an extended radical thoracoabdominal esophagectomy for esophageal cancer, via anterolateral thoracotomy (n=17) or posterolateral thoracotomy (n=13). Patients of both groups were similar in terms of age, sex and preoperative pulmonary function as well as in the anesthetic procedures they have undergone. All patients displayed significantly increased serum levels of IL6 and IL8 after thoracoabdominal esophagectomy. However, patients who were subjected to an anterolateral thoracotomy were reported with significantly higher serum levels of IL6 and IL8 compared to patients who had received a posterolateral thoracotomy. Thus, the choice of the thoracotomy method during the thoracoabdominal esophagectomy and the resultant cytokine levels may contribute to the occurrence of postoperative pulmonary complications and may have an impact on the extent and severity of the surgical stress.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Thoracotomy procedures effect cytokine levels after thoracoabdominal esophagectomy

Frick

Justinger²,

Rubie³

et al. 2011

Oncol Rep

View full text Add to dashboard Cite

show abstract

Section: Epithelial Cell Responses To Mechanical Stretchmentioning

confidence: 99%

“…Additional studies from this trial demonstrated that, in patients with ALI, baseline plasma levels of IL-6, -8 and -10 were associated with increased mortality and a decrease in ventilator-free and organ failurefree days. Patients receiving lower tidal volumes had reduced plasma levels of IL-6 and -8, indicating that ventilatory management can modify circulating inflammatory cytokines [54].Another study of a lung-protective strategy demonstrated reduced lung inflammation and reduced concentrations of inflammatory cytokines in plasma and bronchoalveolar lavage (BAL) fluid associated with a lung-protective strategy [55]. Stuber and colleagues examined the kinetics of cytokine expression associated with tidal volume changes.…”

mentioning

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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“…1995; Parsons et al. 2005). It has also been shown that IL‐6 may be a useful biomarker for stratification of asthma patients by reflecting poor lung function and increased risk for developing exacerbations (Peters et al., 2016).…”

Section: Discussionmentioning

confidence: 99%

Bronchial microdialysis monitoring of inflammatory response in open abdominal aortic aneurysm repair; an observational study

et al. 2017

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Aortic surgery results in ischemia–reperfusion injury that induces an inflammatory response and frequent complications. The magnitude of the inflammatory response in blood and bronchi may be associated with the risk of immediate complications. The purpose of the study was to evaluate bronchial microdialysis as a continuous monitoring of cytokines in bronchial epithelial lining fluid (ELF) and to determine whether bronchial ELF cytokine levels reflect the ischemia–reperfusion injury and risk for complications during open abdominal aortic aneurysm (AAA) repair. We measured cytokines in venous blood using microdialysis and in serum for comparison. Sixteen patients scheduled for elective open AAA repair were included in a prospective observational study. Microdialysis catheters were introduced into a bronchi and a cubital vein. Eighteen cytokines were measured using a Bio‐Plex Magnetic Human Cytokine Panel. Samples were collected before and during cross‐clamping of the aorta as well as from 0 to 60 min and from 60 to 120 min of reperfusion. The ELF levels of several cytokines changed significantly during reperfusion. In particular, IL‐6 increased more than 10‐fold and IL‐13 more than 5‐fold during ischemia and reperfusion. Also, the venous levels of several inflammatory and anti‐inflammatory cytokines increased and exhibited their highest concentration during reperfusion. Both bronchial and venous cytokine levels correlated with duration of the procedure, intensive care days, and preoperative kidney disease. Three patients suffered organ failure as a direct consequence of the procedure, and in these patients the bronchial ELF concentrations of 17 of 18 cytokines differed significantly from patients without such complications. Bronchial microdialysis is suited for continuous monitoring of inflammation during open AAA repair. The bronchial ELF cytokine levels may be useful in predicting immediate complications such as organ failure in patients undergoing vascular surgery.

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Lower tidal volume ventilation and plasma cytokine markers of inflammation in patients with acute lung injury*

Cited by 642 publications

References 36 publications

Thoracotomy procedures effect cytokine levels after thoracoabdominal esophagectomy

Thoracotomy procedures effect cytokine levels after thoracoabdominal esophagectomy

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

Bronchial microdialysis monitoring of inflammatory response in open abdominal aortic aneurysm repair; an observational study

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