Acute respiratory distress syndrome

Chen, Hsing I.; Kao, Shang Jyh; Wang, David; Lee, Ru Ping; Su, Chin Cheng

doi:10.1007/bf02256308

Cited by 39 publications

(21 citation statements)

References 37 publications

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“…In clinical studies, acute hyperglycemia was associated with increased production of inflammatory cytokines and increased mortality rate in critically ill patients, independent of diabetes (26, 27). Hyperglycemia is a risk factor for increased development of ALI in specific disease states, such as Enterovirus infection (28), Coxsackievirus infection (29), and Japanese B encephalitis (30). …”

Section: Resultsmentioning

confidence: 99%

Diabetes, insulin, and development of acute lung injury

Honiden

Gong

2009

Critical Care Medicine

113

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Objectives-Recently, many studies have investigated the immunomodulatory effects of insulin and glucose control in critical illness. This review examines evidence regarding the relationship between diabetes and the development of acute lung injury/acute respiratory distress syndrome (ALI/ARDS), reviews studies of lung injury related to glycemic and nonglycemic metabolic features of diabetes, and examines the effect of diabetic therapies.Data Sources and Study Selection-A MEDLINE/PubMed search from inception to August 1, 2008, was conducted using the search terms acute lung injury, acute respiratory distress syndrome, hyperglycemia, diabetes mellitus, insulin, hydroxymethylglutaryl-CoA reductase inhibitors (statins), angiotensin-converting enzyme inhibitor, and peroxisome proliferatoractivated receptors, including combinations of these terms. Bibliographies of retrieved articles were manually reviewed.Data Extraction and Synthesis-Available studies were critically reviewed, and data were extracted with special attention to the human and animal studies that explored a) diabetes and ALI; b) hyperglycemia and ALI; c) metabolic nonhyperglycemic features of diabetes and ALI; and d) diabetic therapies and ALI.Conclusions-Clinical and experimental data indicate that diabetes is protective against the development of ALI/ARDS. The pathways involved are complex and likely include effects of hyperglycemia on the inflammatory response, metabolic abnormalities in diabetes, and the interactions of therapeutic agents given to diabetic patients. Multidisciplinary, multifaceted studies, involving both animal models and clinical and molecular epidemiology techniques, are essential. Keywordsacute respiratory distress syndrome; acute lung injury; hyperglycemia; diabetes mellitus; insulin Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) is a devastating condition defined by the American-European Consensus Committee on ARDS as an acute syndrome of lung inflammation and increased permeability associated with severe hypoxia and bilateral infiltrates on chest radiographs with no evidence of left heart failure (1). Decades of animal and clinical studies have identified several pathophysiologic mechanisms important in the development of ALI/ARDS. Acute inflammation is a key feature, as evidenced by the central role of neutrophil recruitment and activation and the increased expression and release of inflammatory mediators, such as proinflammatory and antiinflammatory cytokines and chemokines. Disturbances in surfactant function and edema Copyright © 2009 clearance are present, and ample evidence supports imbalances in oxidant/antioxidant activity (2), coagulation/fibrinolysis, and fibrosis/repair. The relative balance of these interacting pathways either exacerbates or ameliorates further lung injury (3,4).ALI/ARDS is a commonly encountered condition, with 190,600 cases of ALI per year in the United States and an associated 74,500 deaths and 3.6 million hospital days (5). Of the predisposing injuries for ALI/ARDS, ...

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Section: Resultsmentioning

confidence: 99%

Diabetes, insulin, and development of acute lung injury

Honiden

Gong

2009

Critical Care Medicine

113

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“…Acute respiratory distress syndrome (ARDS) or acute lung injury (ALI) are major causes of mortality 1,2 . Pulmonary air embolism causes obstruction of the lung microvasculature, resulting in pulmonary hypertension and acute pulmonary oedema 3–5 .…”

Section: Introductionmentioning

confidence: 99%

Nitric Oxide Modulates Air Embolism‐induced Lung Injury in Rats With Normotension and Hypertension

Liu¹,

Kao²,

Chuang³

et al. 2007

Clin Exp Pharma Physio

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1. Air embolism the in lungs induces microvascular obstruction, mediator release and acute lung injury (ALI). Nitrite oxide (NO) plays protective and pathological roles in ALI produced by various causes, but its role in air embolism-induced ALI has not been fully investigated. 2. The purpose of the present investigation was to elucidate the involvement of NO and pro-inflammatory cytokines in the pathogenesis of ALI following air infusion into isolated perfused lungs from spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto (WKY) rats. 3. The extent of ALI was evaluated by changes in lung weight, Evans blue dye leakage, the protein concentration in the bronchoalveolar lavage and pathological examination. We also measured nitrite/nitrate (NO(x)), tumour necrosis factor (TNF)-alpha and interleukin (IL)-1beta concentrations in lung perfusate and determined cGMP in lung tissue. 4. The NO synthase (NOS) inhibitors N(G)-nitro-l-arginine methyl ester (l-NAME) and l-N(6)-(1-iminoethyl)-lysine (l-Nil), as well as the NO donors sodium nitroprusside (SNP) and s-nitroso-N-acetylpenicillamine (SNAP), were administered 30 min before air embolism at a concentration of 10(-3) mol/L in the lung perfusate. 5. Air embolism-induced ALI was enhanced by pretreatment with l-NAME or l-Nil, but was alleviated by SNP or SNAP pretreatment, in both SHR and WKY rats. In both SHR and WKY rats, AE elevated levels of NO(x) (2.6 and 28.7%, respectively), TNF-alpha (52.7 and 158.6%, respectively) and IL-1beta (108.4 and 224.1%, respectively) in the lung perfusate and cGMP levels in lung tissues (35.8 and 111.2%, respectively). Pretreatment with l-LAME or l-Nil exacerbated, whereas SNP or SNAP abrogated, the increases in these factors, except in the case of NO(x) (levels were decreased by l-LAME or l-Nil pretreatment and increased by SNP or SNAP pretreatment). 6. Air embolism caused increases in the lung weight (LW)/bodyweight ratio, LW gain, protein concentration in bronchoalveolar lavage and Evans blue dye leakage. These AE-induced changes were less in lungs isolated from SHR compared with normotensive WKY rats. 7. The results suggest that ALI and associated changes following air embolism in lungs isolated from SHR are less than those in WKY rats. Nitric oxide production through inducible NOS isoforms reduces air embolism-induced lung injury and associated changes. Spontaneously hypertensive rats appear to be more resistant than WKY rats to air embolism challenge.

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“…This serious clinical condition usually results in fatal outcome [26,27]. This serious clinical condition usually results in fatal outcome [26,27].…”

Section: Hypercalcemia and Lung Injurymentioning

confidence: 99%

Biomedical vignette

2008

J Biomed Sci

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Acute respiratory distress syndrome

Cited by 39 publications

References 37 publications

Diabetes, insulin, and development of acute lung injury

Diabetes, insulin, and development of acute lung injury

Nitric Oxide Modulates Air Embolism‐induced Lung Injury in Rats With Normotension and Hypertension

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