Atelectasis Causes Alveolar Injury in Nonatelectatic Lung Regions

Tsuchida, Shinya; Engelberts, Doreen; Peltekova, Vanya; Hopkins, Natalie; Frndova, Helena; Babyn, Paul; McKerlie, Colin; Post, Martin; McLoughlin, Paul; Kavanagh, Brian P.

doi:10.1164/rccm.200506-1006oc

Cited by 206 publications

(148 citation statements)

References 39 publications

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“…All lambs survived to the 3 h study. Pao 2 There were no differences between the LPS and salineexposed CMV groups for Paco 2 , V T , or oxygenation index. The CPAP group exposed to LPS had higher Paco 2 values than the saline-exposed lambs on CPAP, but V T and oxygenation index were similar over the 3 h study.…”

Section: Resultsmentioning

confidence: 74%

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Lung and Systemic Inflammation in Preterm Lambs on Continuous Positive Airway Pressure or Conventional Ventilation

et al. 2009

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Intratracheal lipopolysaccharide (LPS) causes acute inflammation and injurious mechanical ventilation results in pulmonary and systemic inflammation. We aimed to determine in preterm lungs if continuous positive airway pressure (CPAP) protects against pulmonary and systemic inflammation, compared with conventional mechanical ventilation (CMV) after intratracheal LPS. Preterm fetuses were exposed to maternal betamethasone and Epostane 36 h before delivery at 133 d gestational age (term ϭ 150 d). Lambs were intubated and randomized to receive gentle CMV (tidal volume 8 mL/kg) or CPAP with 8 cm H 2 O pressure. Surfactant (10 mg/kg) mixed with 1 mg LPS or saline was instilled into the trachea at 15 min. Blood gas status, ventilation variables, and arterial pressures were recorded for 3 h. Static pressure-volume curves and lung and systemic inflammation were assessed postmortem. CPAP lambs had elevated Paco 2 and minute ventilation compared with the CMV lambs. Cytokine mRNA was increased in the lungs and liver of CPAP and CMV lambs relative to unventilated controls. Intratracheal LPS amplified the cytokine mRNA responses of IL-1␤, IL-6, and IL-8 in the lung and liver. Blood neutrophils decreased similarly after LPS in CPAP and CMV groups. Cytokine markers of lung injury or the systemic response to intratracheal LPS were not decreased by CPAP relative to CMV, in preterm lambs. . Similarly, ventilation with lung volumes that approach or exceed total lung capacity will stretch the lungs and cause injury (3,4). The preterm fetal lung is particularly vulnerable to lung injury during the transition from a fluid-filled lung to airway breathing because surfactant deficiency increases the pressures required to open the lung, the lung aerates nonuniformly, and the delicate tissues of the preterm lung are easily stretched (5,6). The use of continuous positive airway pressure (CPAP) is being advocated for transitioning the preterm fetal lung to air breathing as a way to decrease lung injury (7,8). Although CPAP can cause lung injury in sepsis models (9), CPAP can decrease indicators of lung injury in preterm lambs (10) compared with conventional mechanical ventilation (CMV) and its use has been associated with decreased bronchopulmonary dysplasia (11).Prior exposure of the adult lung to pro-inflammatory mediators such as endotoxin amplifies lung injury caused by ventilation from low lung volumes or elevated lung volumes (9,12,13), and the mediators can enter the systemic circulation and cause systemic inflammatory responses (14,15). Termventilated lambs do not leak endotoxin from the airspaces into the systemic circulation unless the lungs are over-stretched (16). In contrast, preterm lungs leak endotoxin or IL-1 with conventional ventilation (16,17). Chorioamnionitis is associated with many preterm deliveries before 32 wk gestational age, and inflammatory mediators are present in the fetal lung (18,19). We hypothesized that spontaneous breathing with CPAP would protect the preterm lung and minimize a systemic inflamma...

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Section: Resultsmentioning

confidence: 74%

“…M echanical ventilation of lungs from volumes below the normal functional residual capacity (FRC) cause injury by repetitively opening collapsed lung units (1,2). Similarly, ventilation with lung volumes that approach or exceed total lung capacity will stretch the lungs and cause injury (3,4).…”

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confidence: 99%

Lung and Systemic Inflammation in Preterm Lambs on Continuous Positive Airway Pressure or Conventional Ventilation

et al. 2009

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“…Kavanagh showed in a rat model of ARDS/ventilator‐induced lung injury that the major alveolar inflammatory response was localised not in atelectatic regions but in non‐dependent aerated regions. Distal airway injury occurred in both dependent and non‐dependent regions alike 14. Similarly, Terragni et al showed in human patients imaged with CT, that those in whom tidal ventilation was predominantly distributed to hyperaerated lung regions (and who also had larger areas of atelectasis) showed a greater inflammatory response – as measured by pulmonary cytokine concentrations – than those in whom tidal ventilation was predominantly distributed to normally aerated lung (and who also had smaller areas of atelectasis) 15.…”

Section: Dynamic Blood Gas Analysismentioning

confidence: 95%

Intravascular oxygen sensors with novel applications for bedside respiratory monitoring

Formenti

Farmery

2017

Anaesthesia

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SummaryMeasurement allows us to quantify various parameters and variables in natural systems. In addition, by measuring the effect by which a perturbation of one part of the system influences the system as a whole, insights into the functional mechanisms of the system can be inferred. Clinical monitoring has a different role to that of scientific measurement. Monitoring describes measurements whose prime purpose is not to give insights into underlying mechanisms, but to provide information to ‘warn’ of imminent events. What is often more important is the description of trends in measured variables. In this article, we give some examples ‐ focussed around oxygen sensors ‐ of how new sensors can make important measurements and might in the future contribute to improved clinical management.

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“…Sections of 5 m were then stained with hematoxilin and eosin for light microscopic evaluation and scoring. A semi-quantitative analysis of inflammatory cell infiltration was assessed as previously described (20,21) using the following three parameters. Airspace Score: the presence of inflammatory cells in interalveolar septa; and the presence of inflammatory cells within alveoli; and Airway Score: peribronchiolar infiltration of inflammatory cells.…”

Section: B Ronchopulmonary Dysplasia (Bpd) Remains a Majormentioning

confidence: 99%

Lipopolysaccharide Exposure Modifies High Tidal Volume Ventilation-Induced Proinflammatory Mediator Expression in Newborn Rat Lungs

et al. 2007

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Infection/inflammation and mechanical ventilation have both independently been shown to increase cytokine/chemokine levels in lung tissue and blood samples of premature patients. Little is known about the combined effect of systemic inflammation and mechanical ventilation on cytokine expression in the lung. We tested whether pre-existing inflammation induced by lipopolysaccharide (LPS) exposure would modify cytokine/chemokine response in newborn rat lungs to high tidal volume ventilation (HTVV). Newborn rats were randomly assigned to four groups: groups I and II (saline); groups III and IV: 3 mg/kg LPS. Groups II and IV were 24h later subjected to 3h of ventilation with a tidal volume of 25 mL/kg. HTVV alone increased IL-1␤, IL-6 and the chemokine (C-X-C motif) ligand 2 (CXCL2) mRNA expression. Although the cytokine response to LPS alone had disappeared after 24 h, the combination of LPS pretreatment and HTVV significantly increased the expression of IL-6 and IL-1␤ mRNA when compared with HTVV alone. TNF-␣ expression was increased neither by HTVV alone nor in combination with LPS. IL-6 protein content in bronchoalveolar lavage increased due to the combined treatment. Thus, a subtle pre-existing inflammation combined with HTVV amplifies the proinflammatory cytokine/chemokine expression in the newborn rat lung compared with HTVV alone. (Pediatr Res 61: [191][192][193][194][195][196] 2007) B ronchopulmonary dysplasia (BPD) remains a major healthcare problem in neonatology (1). It affects mainly premature babies which require mechanical ventilation and high concentrations of oxygen early in life. Risk is enhanced with an associated infection/inflammation, e.g., chorioamnionitis or sepsis (2,3). The inflammation in BPD is characterized by recruitment of neutrophils from blood into the injured lung tissue that is directed by a group of proinflammatory polypeptides, the chemokines. A subclass of chemokines, the glutamyl-leucyl-arginine (ELR) motif containing CXC chemokines, incuding IL-8 and growth regulated oncogene (GRO), has been shown to be critical for neutrophil binding and chemotactic functions (4). Increased levels of proinflammatory cytokines/chemokines such as IL-8, IL-6 and IL-1␤ in amniotic fluid and bronchoalveolar lavage fluid (BALF) of premature infants have been proposed to be prognostic indicators for developing BPD (5-7). Proinflammatory cytokines/ chemokines are up-regulated by different stimuli, such as mechanical, hyperosmotic or oxidative cellular stress, bacterial or viral products, or other proinflammatory cytokines (8 -10). A few studies in adult rodents have recently investigated the combined effect of pre-existing inflammation and mechanical ventilation on pulmonary cytokine/chemokine expression and injury (11-13). The combination of mechanical ventilation and local (lung) or systemic inflammation showed an increased risk for lung injury. Moreover, expression of the chemokine CXCL2 (GRO2/MIP2, macrophage inflammatory protein 2), a functional rodent homolog of human IL-8, was incr...

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Atelectasis Causes Alveolar Injury in Nonatelectatic Lung Regions

Cited by 206 publications

References 39 publications

Lung and Systemic Inflammation in Preterm Lambs on Continuous Positive Airway Pressure or Conventional Ventilation

Lung and Systemic Inflammation in Preterm Lambs on Continuous Positive Airway Pressure or Conventional Ventilation

Intravascular oxygen sensors with novel applications for bedside respiratory monitoring

Lipopolysaccharide Exposure Modifies High Tidal Volume Ventilation-Induced Proinflammatory Mediator Expression in Newborn Rat Lungs

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