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ISRN Physiology 2013
Macromolecule Permeability in Rodent Intestine following Thermal Injury and Lipopolysaccharide ChallengeDOI: 10.1155/2013/362856 Abstract: The barrier function of the intestinal mucosa may be lost during stress such as severe trauma and sepsis. The present study utilized a multicannulated (jugular vein, proximal jejunum, thoracic duct, and portal vein) rat model of burn (30% body surface area (TBSA)) and endotoxemia (E. coli lipopolysaccharide (LPS) infused via the jugular cannula) to investigate in vivo barrier function to macromolecules with different sizes and the route for their transport (horse radish peroxidase (HRP) and 14C-polyethylene glycol (PEG)-4,000 infused via jejunal cannula). In burn rats, mucosa uptakes of HRP and PEG increased 3?h after their intraluminal infusion compared to the controls. Studies with intravenous 111In-IgG infusion showed that its recovery in small intestine was decreased after burn and LPS infusion, indicating that blood perfusion to intestine was compromised. The present study suggests that (1) burn and endotoxemia increase intestinal permeability to macromolecules; (2) the portal blood may be the major route of transport for molecules up to sizes of 4,000 during burn but not endotoxemia; and (3) intestinal hypoperfusion could be one of the factors that contribute to increased gut permeability in severe burn trauma and sepsis. 1. Introduction In addition to its role in nutrient absorption, the intestinal mucosa functions as a major barrier to the passage of infectious and/or potentially toxic macromolecules present in the gut lumen. However, this barrier function may be lost under certain circumstances, such as hemorrhagic shock, severe trauma, and sepsis, leading to the subsequent development of systemic sepsis and multiple organ failure syndrome [1, 2]. It has been demonstrated in animal model in vivo that endotoxin and thermal injury could induce bacterial translocation from gut lumen to mesenteric lymph nodes, liver, or spleen [3, 4]. We have previously shown that, using the everted intestinal sac model in vitro, 20% body surface area (BSA) thermal injury enhances the small intestinal permeability to a variety of macromolecules such as horse radish peroxidase and polyethylene glycol [5]. We have also demonstrated that there is a markedly diminished in vivo incorporation of tritiated thymidine into the small intestinal mucosa for a transient period after these injuries [6]. In the present study, we established a multiple cannulated whole animal model to investigate the intestinal barrier function during stress and the possible routes of macromolecule passage after they penetrate the intestinal mucosa. 2. Materials and Methods 2.1. Animals All
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