Bacterial Translocation in a Large-Animal Model of Small-Bowel Transplantation

Fryer, Jonathan P.; Kim, Sung Hoon; Wells, Carol L.; Fasola, Carlos G.; Jechorek, Robert P.; Dünn, David L.; Pirenne, Jacques; Arazola, Luis; Gruessner, Rainer W.G.

doi:10.1001/archsurg.1996.01430130079016

Cited by 30 publications

(2 citation statements)

References 26 publications

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“…Although bacteria in the gut can be a potential injury mechanism for the intestine (Yale 1969; Musemeche et al 1986; Deitch et al 1991), they tend to be distributed throughout the gut with higher levels in the ileum regions compared to the jejunum (Salanitro et al 1978; Fryer et al 1996). However, the intestinal injury was greatest at locations where food boluses were present and where digestive enzymes are most concentrated.…”

Section: Discussionmentioning

confidence: 99%

Removal of luminal content protects the small intestine during hemorrhagic shock but is not sufficient to prevent lung injury

et al. 2013

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The small intestine plays a key role in the pathogenesis of multiple organ failure following circulatory shock. Current results show that reduced perfusion of the small intestine compromises the mucosal epithelial barrier, and the intestinal contents (including pancreatic digestive enzymes and partially digested food) can enter the intestinal wall and transport through the circulation or mesenteric lymph to other organs such as the lung. The extent to which the luminal contents of the small intestine mediate tissue damage in the intestine and lung is poorly understood in shock. Therefore, rats were assigned to three groups: No-hemorrhagic shock (HS) control and HS with or without a flushed intestine. HS was induced by reducing the mean arterial pressure (30 mmHg; 90 min) followed by return of shed blood and observation (3 h). The small intestine and lung were analyzed for hemorrhage, neutrophil accumulation, and cellular membrane protein degradation. After HS, animals with luminal contents had increased neutrophil accumulation, bleeding, and destruction of E-cadherin in the intestine. Serine protease activity was elevated in mesenteric lymph fluid collected from a separate group of animals subjected to intestinal ischemia/reperfusion. Serine protease activity was elevated in the plasma after HS but was detected in lungs only in animals with nonflushed lumens. Despite removal of the luminal contents, lung injury occurred in both groups as determined by elevated neutrophil accumulation, permeability, and lung protein destruction. In conclusion, luminal contents significantly increase intestinal damage during experimental HS, suggesting transport of luminal contents across the intestinal wall should be minimized.

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Section: Discussionmentioning

confidence: 99%

Removal of luminal content protects the small intestine during hemorrhagic shock but is not sufficient to prevent lung injury

et al. 2013

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“…23 Pneumonia was the main infectious complication in this pig model. In group 2 all pigs lived for more than 20 days.…”

Section: Discussionmentioning

confidence: 79%

Allograft Rejection of Small Bowel Transplantation in Pigs

et al. 1998

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Small bowel allograft rejection in large animals has yet to be well defined. There are no specific early signs of graft rejection. The present experiments were undertaken to compare acute small bowel allograft rejection in pigs with and without FK506 and also to examine the usefulness of mucosal biopsies. Thirty-six outbred Large-White pigs were divided into (1) group 1 (n = 9): nonimmunosuppressed recipients; (2) group 2 (n = 8): FK506-immunosuppressed recipients; (3) group 3 (n = 2): autotransplant controls; and (4) donors (n = 17). Orthotopic small bowel transplantations were performed with Thiry-Vella loops for daily biopsies. The survival rate of group 2 was significantly longer than that of group 1 (P < 0.05). One best survivor in group 2 was killed at postoperative day (POD) 365. Treatment by FK506 prevented rejection, but most of the pigs died of pneumonia. In group 1, rejection began on POD 3 and progressed to severe rejection rapidly within 7 days. In group 2, rejection began from POD 6 to POD 8, but either remained mild or spontaneously improved. The differences in the routine laboratory data and the tumor necrosis factor-alpha level were not evident between the groups. Histological studies of repeated graft biopsies are thus considered to be essential for detecting signs of graft rejection.

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