Reduction in Biliary IgA After Burn Injury

Cappeller, W. A.; Bloch, Kurt J.; Hatz, R.; Carter, E A; Fagundes, J J; Sullivan, David A.; Harmatz, Paul

doi:10.1097/00000658-199204000-00006

Cited by 3 publications

(3 citation statements)

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“…The intestinal IgA levels appear to be associated with the local immunological dysfunction [38][39][40][41] . The change in intestinal pHi showed that intestinal hemorrhagic injury may result in the release of intestinal mucosal enzyme, subsequently leading to significant elevation of plasma DAO activity.…”

Section: Discussionmentioning

confidence: 99%

Preventive effect of glutamine on intestinal barrier dysfunction induced by severe trauma

Li¹,

Lü²,

Hu³

et al. 2002

WJG

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AIM: To investigate the mechanism underlying intestinal barrier function damage after severe trauma and the therapeutic effect of glutamine. METHODS:Burned patients, and animal models of severe trauma replicated by hemorrhagic shock combined with endotoxin infusion and burn injury, were included in a serial experiment. Effects of oral glutamine on intestinal barrier function were observed in scalded rats. Parameters measured in these experiments were as follows: plasma levels of diamine oxidase (DAO), tumor necrosis factor (TNFα α α α α), endotoxin (LPS), and lactate as well as D-lactate by biochemical methods, lactose/mannitol (L/M) ratio in urine by SP-3400, and pathological examination of intestinal mucosa under light microscopy. RESULTS: INTRODCTIONIt is generally accepted that the intestine may serve as an important organ in the development of severe complications under critically ill conditions, including trauma, burns, shock, etc.[1-3] Hemorrhagic shock and/or gut ischemia-reperfusion injury commonly occur in the early stage after acute insults, leading to gut-derived sepsis as a result of gut barrier dysfunction [4][5][6][7][8][9][10] . In order to investigate the mechanism underlying intestinal barrier function damage and its potential interventional measures, burned patients and animal models of severe trauma were employed in our current experiments [6,[11][12][13][14][15] . MATERIALS AND METHODS Animal modelsAnimal models of severe trauma were replicated by hemorrhagic shock combined with endotoxin infusion. Male Wistar rats, weighing 190g-230g, were anaesthetized with intraperitoneal injection of 30g·L -1 barbitone sodium (35mg·kg -1 ), and the femoral artery and jugular vein were cannulated under aseptic conditions. The rats were then bled via the jugular vein catheter until a mean arterial pressure of 30-35 mmHg (4.6 kPa) was reached. At the end of shock, endotoxin (E.coliO55 B5, Sigma) was infused through tail vein at a dose of 2mg·kg -1 . A goat model of hemorrhagic shock combined with endotoxin challenge was established according to the previous report(n=20) [5] . Animals received E.coliO26 B6 endotoxin via portal vein 24h after the recovery from shock, and the dosage was 30 ng·kg -1 ·min -1, which was given in a continuous infusion lashing for 5d. Wistar rats were divided randomly into three groups: normal controls, early feeding with standard feed plase Gln 0.5g after scalding, and animals (except control group) sustained a 30% TBSA fullthickness scald covering the back and flanks [6] . Determination of plasma diamine oxidase in 21 burned patients (17 male and 4 female) at the age of 33±10 years, with burn area (64±21)%, and (35±20)% 0. Plasma DAO activity was determined on day 1, 3, 7, 14 and 21 postburn.Blood and intestinal DAO levels were tested according to our previous report [17] . Plasma lactate and Dlactate concentrations were determined by biochemical methods as described by Brandt et al [18] . Microassay for quantitation of endotoxin in blood was made with new PCA treatment...

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Section: Discussionmentioning

confidence: 99%

Preventive effect of glutamine on intestinal barrier dysfunction induced by severe trauma

Li¹,

Lü²,

Hu³

et al. 2002

WJG

View full text Add to dashboard Cite

show abstract

“…En general, se considera que son necesarios todos estos factores para que la translocación bacteriana llegue a producirse. El sobrecrecimiento bacteriano intestinal desempeña un papel muy importante en la patogenia de la translocación bacteriana 2,10,11,14 y estaría favorecido por diversos factores como las alteraciones en los mecanismos de defensa inmunológica locales 15,16 , la disminución en la motilidad intestinal 13 , la administración prolongada de antibióticos que determinaría el sobrecrecimiento de bacterias resistentes 17,18 o la malnutrición 2 . Entre los mecanismos de defensa inmunológica locales frente al desarrollo de translocación bacteriana son de especial importancia las placas de Peyer, los linfocitos y macrófagos de la pared intestinal y la producción de IgA local y excretada con la bilis 1 .…”

Section: Patogenia De La Translocación Bacterianaunclassified

“…Entre los mecanismos de defensa inmunológica locales frente al desarrollo de translocación bacteriana son de especial importancia las placas de Peyer, los linfocitos y macrófagos de la pared intestinal y la producción de IgA local y excretada con la bilis 1 . En este sentido, se ha observado una disminución de la producción de IgA en la bilis de ratas con quemaduras 16 y en el intestino de pacientes con cirrosis alcohólica 15 , que podría contribuir al desarrollo de translocación bacteriana en estas situaciones. A nivel sistémico, se han descrito múltiples alteraciones en los mecanismos de defensa inmunológica 1,11 en las diferentes situaciones en que se produciría la translocación bacteriana, destacando la disminución en la actividad del sistema reticuloendotelial 19 , la disfunción en la actividad fagocítica de los neutrófilos 20 y la disminución en la concentración de diversas proteínas del suero con actividad opsónica 1,21 .…”

Section: Patogenia De La Translocación Bacterianaunclassified