Pulmonary Endothelial Permeability in Patients With Severe Lung Injury

Sinclair, D. G.; Braude, S.; Haslam, P L; Evans, Timothy W.

doi:10.1378/chest.106.2.535

Cited by 75 publications

(35 citation statements)

References 21 publications

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“…At the onset of ARDS, we have found BAL albumin and total protein levels to be similar in survivors and nonsurvivors. In agreement with others [144,147], we noted survivors to have a progressive decline in BAL albumin and total protein levels over time (not seen in nonsurvivors), suggesting effective repair of the alveolar-endothelial surface [50]. We have also identified a consistent correlation between BAL albumin and total protein levels and BAL TNF-α, IL-1β, IL-6 and IL-8 levels [50].…”

Section: Pulmonary Vascular Permeabilitysupporting

confidence: 91%

“…HOST DEFENCE RESPONSE AND OUTCOME IN ARDS ARDS, by day 3-7 clearly separated survivors (increased) from nonsurvivors (decreased or no change) [50,108,[138][139][140][141][142][143][144][145]. In one report, mortality rate in patients with and without improvement in lung function by day 7 of ARDS was 43 and 97%, respectively [141].…”

Section: Gas Exchange and Lung Mechanicsmentioning

confidence: 99%

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The role of the host defence response in the progression and outcome of ARDS: pathophysiological correlations and response to glucocorticoid treatment

Gu¹

1996

Eur Respir J

114

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T Th he e r ro ol le e o of f t th he e h ho os st t d de ef fe en nc ce e r re es sp po on ns se e i in n t th he e p pr ro og gr re es ss si io on n a an nd d o ou ut tc co om me e o of f A AR RD DS S: : p pa at th ho op ph hy ys si io ol lo og gi ic ca al l c co or rr re el la at ti io on ns s a an nd d r re es sp po on ns se e t to o g gl lu uc co oc co or rt ti ic co oi id d t tr re ea at tm me en nt t

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Section: Pulmonary Vascular Permeabilitysupporting

confidence: 91%

Section: Gas Exchange and Lung Mechanicsmentioning

confidence: 99%

The role of the host defence response in the progression and outcome of ARDS: pathophysiological correlations and response to glucocorticoid treatment

Gu¹

1996

Eur Respir J

114

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“…2 The large amount of toxic reactive oxygen species and granule enzymes released from neutrophils can cause catastrophic collateral damage to host tissues. 3 Interleukin-18 is a pro-inflammatory cytokine that induces γ-interferon (IFN-γ) production; IL-18 is also known as an inflammasome that is activated by the caspase-1 pathway. Recent studies suggest that inflammasome-related cytokines, including IL-18, play important roles in acute lung injury.…”

Section: Introductionmentioning

confidence: 99%

Role of endogenous IL‐18 in the lung during endotoxin‐induced systemic inflammation

Takahara

Ishikawa

Shuno

et al. 2013

Acute Medicine & Surgery

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Background: Overactivated neutrophils are causes of acute lung injury, which is a major clinical problem with significant morbidity and mortality in sepsis. Serum interleukin (IL)-18 levels correspond to severity of systemic inflammation.Aim: To elucidate the roles of endogenous IL-18 in lung injury during endotoxin-induced systemic inflammation. Methods: Wild-type (WT) and IL-18 gene knockout (KO) mice were injected with lipopolysaccharide (40 mg/kg) intraperitoneally and killed. Lungs were collected at 0 and 12 h to assess mRNA for intercellular adhesion molecule (ICAM)-1, inducible nitric oxide synthase, myeloperoxidase, immunohistochemistry (cleaved caspase-3, 8-hydroxy-2-deoxyguanosine), and wet/dry ratio. Blood was collected at 0, 1, 12, 18, and 24 h to assess plasma cytokine levels. Results:The survival rates at 24 h were approximately 43% and 76% in the WT and KO mice, respectively. Plasma IL-18 levels were induced time-dependently only in the WT mice. Plasma interferon-γ levels were significantly higher in the WT than in the KO mice at 12 h, but IL-6 and tumor necrosis factor-α levels did not differ between the WT and KO mice. At 12 h, the WT mice showed higher myeloperoxidase activity (P < 0.05), ICAM-1, and wet/dry ratios than KO mice. Cleaved caspase-3 positive neutrophils, which migrated in the lung interstitium, were lower in WT mice than in KO mice.Conclusions: Endogenous IL-18 induced neutrophil accumulation, accompanied by induction of ICAM-1 expression, inhibition of neutrophil apoptosis, and increased inducible nitric oxide synthase-induced oxidative tissue injury in the lung, leading to lung edema and poor outcome during endotoxemia.

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“…Measurements of changes in alveolar capillary permeability have been made in patients with ARDS over protracted periods. An increase in pulmonary vascular permeability has been shown to not only persist throughout the course of ARDS but also correlate with a clinical score of injury severity and the bronchoalveolar lavage fluid neutrophil content [18].…”

Section: Vascular Permeabilitymentioning

confidence: 99%

The pathogenesis of lung injury following pulmonary resection

Jordan¹,

Mitchell²,

Quinlan³

et al. 2000

Eur Respir J

235

115

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Postpneumonectomy pulmonary oedema (PPO) develops in~5% of patients undergoing pneumonectomy or lobectomy, and has a high associated mortality (>50%). In its extreme form, PPO follows a clinical and histopathological course indistinguishable from acute respiratory distress syndrome.Perioperative fluid overload, impaired lymphatic drainage following node dissection and trauma caused by surgical manipulation have been implicated in the pathogenesis of PPO. However, PPO more probably represents the pulmonary manifestation of a panendothelial injury consequent upon inflammatory processes induced by the surgical procedure, which involves collapse and re-expansion of the operative lung to permit hilar dissection and pulmonary resection.High inspired oxygen concentrations are required to overcome the effects of shunt. Animal studies have shown that pulmonary ischaemia/reperfusion can result in oedema formation, possibly due to the generation of pro-oxidant forces. Moreover, plasma taken from patients undergoing lobectomy or pneumonectomy (but not lesser resections) shows evidence of oxidative damage.Such evidence suggests either that the high inspired oxygen concentrations associated with one-lung ventilation, or ischaemia/reperfusion injury, may modulate postpneumonectomy pulmonary oedema. Mechanisms by which redox imbalance may result in tissue damage and postpneumonectomy pulmonary oedema are discussed. Eur Respir J 2000; 15: 790±799.

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Pulmonary Endothelial Permeability in Patients With Severe Lung Injury

Cited by 75 publications

References 21 publications

The role of the host defence response in the progression and outcome of ARDS: pathophysiological correlations and response to glucocorticoid treatment

The role of the host defence response in the progression and outcome of ARDS: pathophysiological correlations and response to glucocorticoid treatment

Role of endogenous IL‐18 in the lung during endotoxin‐induced systemic inflammation

The pathogenesis of lung injury following pulmonary resection

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