Source:http://linkedlifedata.com/resource/pubmed/id/10390387
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1999-8-11
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pubmed:abstractText |
We examined the hypothesis that injurious ventilatory strategies (large tidal volume [VT] and/or low positive end-expiratory pressure [PEEP]) would increase release of inflammatory mediators into the lung and into the systemic circulation in a lung injury model. Lung injury was induced in 40 anesthetized paralyzed Sprague-Dawley rats (350 +/- 2 g) by hydrochloric acid instillation (pH 1.5, 2.5 ml/kg). Rats were then randomized into five groups (n = 8): (1) high-volume zero PEEP (HVZP): VT, 16 ml/ kg; (2) high-volume PEEP (HVP): VT, 16 ml/kg, PEEP, 5 cm H2O; (3) low-volume zero PEEP (LVZP): VT, 9 ml/kg; (4) low-volume PEEP (LVP): VT, 9 ml/kg, PEEP, 5 cm H2O; (5) same settings as (4) plus a recruitment maneuver performed every hour (LVPR). Respiratory rate was adjusted to maintain normocapnia and fraction of inspired oxygen (FIO2) was 1. Cytokine concentrations (tumor necrosis factor-alpha [TNF-alpha] and macrophage inflammatory protein-2 [MIP-2]) were measured by ELISA. All animals in the LVZP group died before the end of the experiment. After 4 h of ventilation, the HVZP group had similar lung fluid TNF-alpha concentrations compared with the HVP group: 1,861 +/- 333 pg/ml versus 1,259 +/- 189 pg/ml; and much higher serum concentrations: 692 +/- 74 pg/ml versus 102 +/- 31 pg/ml (p < 0.05). An identical pattern was found for MIP-2. These results suggest that the particular ventilatory strategy can affect the release of cytokines into the systemic circulation, a finding that may have relevance for the development of multisystem organ failure.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CXCL2,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Inflammation Mediators,
http://linkedlifedata.com/resource/pubmed/chemical/Monokines,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
1073-449X
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
160
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
109-16
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:10390387-Animals,
pubmed-meshheading:10390387-Chemokine CXCL2,
pubmed-meshheading:10390387-Cytokines,
pubmed-meshheading:10390387-Disease Models, Animal,
pubmed-meshheading:10390387-Inflammation Mediators,
pubmed-meshheading:10390387-Lung,
pubmed-meshheading:10390387-Monokines,
pubmed-meshheading:10390387-Multiple Organ Failure,
pubmed-meshheading:10390387-Positive-Pressure Respiration,
pubmed-meshheading:10390387-Rats,
pubmed-meshheading:10390387-Rats, Sprague-Dawley,
pubmed-meshheading:10390387-Respiration, Artificial,
pubmed-meshheading:10390387-Respiratory Distress Syndrome, Adult,
pubmed-meshheading:10390387-Respiratory Mechanics,
pubmed-meshheading:10390387-Systemic Inflammatory Response Syndrome,
pubmed-meshheading:10390387-Tumor Necrosis Factor-alpha
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pubmed:year |
1999
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pubmed:articleTitle |
Mechanical ventilation affects local and systemic cytokines in an animal model of acute respiratory distress syndrome.
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pubmed:affiliation |
Division of Respiratory Medicine, Mount Sinai Hospital, Samuel Lunenfeld Research Institute, University of Toronto, Toronto, Ontario, Canada.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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