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American journal of physiology. Lung cellular and molecular physiology, 2003-01, Vol.284 (1), p.224-L231
2003
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Autor(en) / Beteiligte
Titel
Induction of endotoxin tolerance improves lung function after warm ischemia in dogs
Ist Teil von
  • American journal of physiology. Lung cellular and molecular physiology, 2003-01, Vol.284 (1), p.224-L231
Ort / Verlag
United States
Erscheinungsjahr
2003
Quelle
MEDLINE
Beschreibungen/Notizen
  • 1  Thoracic and Cardiovascular Surgery, 3  Institute of Epidemiology, Biometrics and Informatics, Martin-Luther-University, 06097 Halle; and 2  Clinical Research Group Shock and Multiorgan Failure, Essen University, 45128 Essen, Germany In shock models, induction of endotoxin tolerance (ET) is known to have a protective effect. The present study was designed to explore if ET is effective in protecting lungs from reperfusion injury. Twelve foxhounds were used as experimental animals. After a left thoracotomy, the left hilum was clamped for 3 h, followed by 8 h of reperfusion. In the treatment group (ET, n  = 6), dogs were pretreated with incremental daily endotoxin doses of up to 60 µg/kg on day 6 . The ischemia and reperfusion experiment was carried out on day 9 . Control group animals ( n  = 6) were not subjected to endotoxin. After 8 h of observation, functional parameters of the reperfused lung of the ET and the control group were statistically different ( P  < 0.05) with respect to P O 2 [ET vs. control: 172.7   ± 12.9 vs. 66.1 ± 7.2 (SE) mmHg], compliance (16.0 ± 1.2 vs. 8.3   ± 1.0 ml/0.1 kPa), and the wet-to-dry ratio (9.4 ± 0.8 vs. 16.7   ± 1.2). After 3 h of warm ischemia and 8 h of reperfusion, pulmonary function and lung water content improved in the endotoxin-tolerant group. ischemia-reperfusion; acute respiratory distress syndrome; surfactant; lipopolysaccharide

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