Alterations in Mucosal Morphology and Permeability, but No Bacterial or Endotoxin Translocation Takes Place After Intestinal Ischemia and Early Reperfusion in Pigs

Schlichting, Ellen; Grotmol, Tom; Kähler, Hanne; Næss, Oddvar; Steinbakk, Martin; Lyberg, Torstein

doi:10.1097/00024382-199502000-00006

Cited by 25 publications

(7 citation statements)

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“…The confocal laser scanning fluorescence microscopic pictures in the present study also give evidence for an enhanced paracellular tissue infiltration of FITC-LPS under hypoxic conditions. However, these findings are somehow in contrast to other studies performed in pigs, showing alterations in mucosal morphology and permeability, but not an enhanced translocation of bacteria or endotoxin after intestinal ischemia and early reperfusion [19]. In our study, there is a clear infiltration of the tissue by fluorescence-labelled endotoxin under hypoxic conditions.…”

Section: Discussioncontrasting

confidence: 99%

Effect of ischemia on intestinal permeability of lipopolysaccharides

Drewe

Beglinger

Fricker

2001

Eur J Clin Investigation

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The enteral absorption of endotoxin (lipopolysaccharide, LPS) was studied in vitro and in vivo. The absorption of fluorescence (FITC) labelled LPS was investigated by uptake studies with rabbit jejunal brush-border membrane vesicles (BBMV), the human intestinal cell line Caco-2 and in rats. FITC-LPS from Salmonella typhimurium was taken up into BBMV in a dose-dependent manner. Uptake was neither pH- nor Na+-dependent, nor could it be inhibited by unlabelled LPS. 74.5% of vesicle-associated fluorescence was due to adhesion to the vesicular membranes, 25.5% was taken up into an osmotically-sensitive space. Transport of LPS across Caco-2 cell monolayers was dose-dependent. The permeation rate increased significantly under ischemic conditions, i.e. when the cells were incubated under oxygen-depleted conditions. However, no significant differences in transepithelial electrical resistances were observed between oxygen depleted and control cells. The release of lactate dehydrogenase was only marginally different from control cells, indicating cell integrity. In situ, after gut ischemia, a significantly increased uptake of fluorescent LPS was observed by fluorescence laser scanning microscopy. Conclusion LPS is taken up by the intestinal mucosa, predominantly by passive transcellular diffusion. Under ischemic conditions, the permeability of LPS is increased mainly by an enhanced paracellular permeability and epithelial destruction. The findings partly explain the clinically observed development of multiorgan system failure after temporary malperfusion of the gut during major vascular surgery or thromboembolism.

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Section: Discussioncontrasting

confidence: 99%

Effect of ischemia on intestinal permeability of lipopolysaccharides

Drewe

Beglinger

Fricker

2001

Eur J Clin Investigation

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“…Duration of visceral ischemia has hereby been recognized to be the primary determinant of subsequent multiple organ failure ( 2–4). Experimentally, mesenteric ischemia is associated with damage to the intestinal mucosa and decreased gut barrier function ( 5). Gut luminal toxins are hereby suspected to trigger a systemic inflammatory response ( 6, 7) which may promote serious septic complications and ultimately lead to multiple organ dysfunction and death.…”

mentioning

confidence: 99%

Supraceliac aortic cross‐clamping and declamping. Effects of dopexamine and dopamine on systemic and mesenteric hemodynamics, metabolism and intestinal tonometry in a rat model

Studer

2000

Acta Anaesthesiol Scand

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“…While an association of endotoxemia with hemorrhage, trauma, and/or operative stress were found by number of authors [5,6,[22][23][24][25], the lack of detectable plasma LPS levels were reported by others [9,26]. Recent evidence suggests that mesenteric lymph rather than the portal circulation may be the main route for cardivascular cell activating factors to reach the peripheral organs, thus, leading to the development of distant organ injury after gut barrier breakdown [11,27].…”

Section: Discussionmentioning

confidence: 99%

Immunoglobulin Enriched Colostral Milk Reduces Gut-Derived Endotoxemia in a Rat Hemorrhage Model

Fitzal

Rácz²,

Hamar³

et al. 2001

Eur J Trauma

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Background: Several studies indicate that a breakdown of mucosal barrier is often a major cause of endotoxemia and septic complications after hemorrhagic/traumatic insults. The aim of this study was to investigate, whether enteral administration of an immunoglobulin enriched colostral milk preparation (ICM) is able to affect endotoxemia as well as survival in a hemorrhagic shock model in rats. Materials and Methods: Rats were orally pre-treated with either 5 ml of 0.9% saline (CON) or ICM (3 g/kg body weight) once a day for 5 days (ICM). Laboratory control animals were not treated (LAB-CON). On day 6, intestinal endotoxin contents were assessed. In a separate set of animals treated similarly, hemorrhage was induced on the 6th day by bleeding the animals to a mean arterial pressure of 30-35 mm Hg for 3 h followed by resuscitation over 1 h. Results: Pre-treatment with ICM significantly reduced intraluminal endotoxin contents in the duodenum when compared with CON (0.43 ± 0.27 vs. 1.03 ± 0.67 EU/mg contents; p = 0.03). Hemorrhage for 3 h resulted in a significant rise in plasma endotoxin concentrations in CON animals compared with LAB-CON (0.30 ± 0.20 vs. 0.06 ± 0.04 EU/ml). ICM pre-treatment attenuated plasma endotoxin levels after hemorrhage (0.11 ± 0.12 EU/ml). The 6-day-survival rate after hemorrhage tended to be higher in the ICM pre-treated animals when compared with CON (66.7% vs. 40%). Conclusion: A passive immunization of the gut together with the reduction of the intraluminal endotoxin contents by enteral administration of immunoglobulin-enriched preparations might prove to be a prophylactic approach towards preventing gut-derived endotoxemia after hemorrhagic/traumatic insults.

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Alterations in Mucosal Morphology and Permeability, but No Bacterial or Endotoxin Translocation Takes Place After Intestinal Ischemia and Early Reperfusion in Pigs

Cited by 25 publications

References 0 publications

Effect of ischemia on intestinal permeability of lipopolysaccharides

Effect of ischemia on intestinal permeability of lipopolysaccharides

Supraceliac aortic cross‐clamping and declamping. Effects of dopexamine and dopamine on systemic and mesenteric hemodynamics, metabolism and intestinal tonometry in a rat model

Immunoglobulin Enriched Colostral Milk Reduces Gut-Derived Endotoxemia in a Rat Hemorrhage Model

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