Table of Contents
ISRN Physiology
Volume 2013, Article ID 362856, 7 pages
Research Article

Macromolecule Permeability in Rodent Intestine following Thermal Injury and Lipopolysaccharide Challenge

1Rhode Island Hospital, Brown University School of Medicine, SWP-511, 593 Eddy Street, Providence, RI 02903, USA
2Departments of Surgery and Pediatrics, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02114, USA
3Massachusetts General Hospital, Pediatric Gastrointestinal Unit, 114 16th Street (114-3503), Charlestown, MA 02129-4004, USA

Received 30 April 2013; Accepted 30 May 2013

Academic Editors: K. Shirasuna, A. Tse, and D. Xiao

Copyright © 2013 Peirong Yu and Edward A. Carter. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.