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S19Vol. 209, No. 3S, September 2009 Surgical Forum Abstracts

ONCLUSIONS: RYGB reduces brush border glucose transport inhe Roux and common channel segments by a mechanism involvingecreased SGLT1 expression. Decreased expression of PEPCK and6Pase suggests intestinal gluconeogenesis is reduced after RYGB asell. These findings enhance our understanding of how RYGB im-roves glucose homeostasis.

echanical stretch aggravates lipopolysaccharide-nduced inflammatory pathways in intestinalmooth muscle cells and macrophagesven Wehner PhD, Anatol Rocke, Silke Schuchtrup, Tim Vilz MD,ndreas Hirner MD, Joerg C Kalff MD, FACSniversity of Bonn, Bonn, North Rhine-Westphalia, Germany

NTRODUCTION: Mechanical trauma is an iatrogenic consequencef abdominal surgery that results in massive inflammation of theunica muscularis, subsequently leading to postoperative ileus (POI).

acrophages and smooth muscle cells (iSMCs) are key players ineveloping POI. The aim of this study was to investigate the inflam-atory response of both cell types to mechanical strain and lipopoly-

accharide (LPS).

ETHODS: Peritoneal macrophages and iSMCs were mechanicallytretched in the presence or absence of LPS or gadolinium with thelexcell tension system. Gene expression of iNOS, COX-2, IL-6, andL-1beta was analyzed by quantitative PCR. Furthermore, mediarom stretched iSMC were transferred to unstretched macrophagesnd vice versa. Proinflammatory gene expression was analyzed in thecceptor cells.

ESULTS: iSMCs significantly up-regulated iNOS (15-fold),OX-2 (2.3-fold), and IL-1beta (3.5-fold) but not IL-6 in response

o stretch. This effect was blocked by gadolinium. In macrophages,ll genes significantly increased by stretch. Both cell types liberatednflammatory mediators and mutually stimulated the expression ofNOS and COX-2 and MIP-2. Stretch potentiates LPS-inducedNOS (244- vs 1250-fold) and IL-1beta (88- vs 421-fold) expressionn iSMCs and COX-2 (77- vs 172-fold), IL-6 (133- vs 313-fold), and

IP-2 (83- vs 172-fold) in macrophages.

ONCLUSIONS: Mechanical strain induces the expression ofroinflammatory genes and the liberation of paracrine-acting proin-lammatory mediators and potentiates LPS-induced gene expressionn iSMCs and macrophages. Further knowledge and inhibition of thetretch-induced signaling cascade is a promising target for preventionf postoperative ileus.

haracterization of tight and adherens junctions inn inflammation model of cultured humaneritoneal mesothelial cellsarkus Utech MD, Mihail Dudarov, Bettina Loeffler MD,orbert Senninger MD, Matthias Bruewerniversity Hospital Muenster, Muenster, North Rhine-Westphalia,ermany

NTRODUCTION: The pathogenesis of intraabdominal adhesion is

omplex and as yet incompletely investigated. Inflammatory pro- t

esses of the peritoneum mediated by proinflammatory cytokinesodulate the formation of intraabdominal adhesion. Cell-cell con-

acts of human peritoneal mesothelial cells (HMCs) are regulated byspecialized plasma membrane structure called the apical junctionalomplex (AJC) that is composed of the tight junction (TJ) and theubjacent adherens junction (AJ). The distribution of TJ and AJ inMCs modulated by proinflammatory cytokines remains unknown.

ETHODS: HMCs were isolated from omental tissue of patientsndergoing elective surgery. The HMCs were seeded onto permeableolycarbonate filters and incubated for 24 hours with interferonIFN)-gamma or interleukin (IL)-1beta. TJ and AJ proteins occlu-in, zonula occludens (ZO)-1, beta-catenin, and claudins 1 and 3ere examined by immunofluorescence microscopy and Westernlot.

ESULTS: In cultured HMCs, all TJ and AJ proteins were physio-ogically located at the apical membrane in a typical chicken-wireattern. After 24 hours of Il-1beta or IFN-gamma incubation, oc-ludin, ZO-1, claudins 1 and 3, and the AJ protein beta-catenin werenternalized from the lateral membrane. Claudin 3 expression was-fold increased by IL-1beta incubation, whereas occludin expres-ion was reduced by IFN-gamma and IL-1beta.

ONCLUSIONS: We observed disturbed distribution and alteredxpression of TJ and AJ proteins induced by proinflammatory cyto-ines in cultured HMCs. Loss of cell-cell contacts mediated byroinflammatory cytokines maybe facilitates connective tissue struc-ures of the lamina propria serosae (such as fibroblasts) to reach theurface of the peritoneum and, thus, may trigger early processes ofntraabdominal adhesion.

ranslational research: The use of rapid samplingicrodialysis for bedside monitoring of bowel

schemiaamer Deeba MD, MRCS(Eng), Emma Corcoles MS,eorge B Hanna MBBS, FRCS, Martyn Boutelle PhD,ra Darzi MD, FACS

mperial College London, London, England

NTRODUCTION: Intestinal ischemia is a major cause of anasto-otic leak and death. It remains a clinical challenge as the physician

elies on several nonspecific signs, biologic markers, and radiologictudies to make the diagnosis. We propose a quantitative noviceedside analysis system that uses rapid sampling microdialysis andnalyzes automatically for real-time concentration changes of intra-ural bowel glucose and lactate as ischemia sets in.

ETHODS: Two studies were conducted in which this apparatusroved its efficacy in real-time monitoring of intestinal ischemiantraoperatively in a segment of colon being resected and in moni-oring a swine model of bowel anastomosis. The apparatus is noweing deployed at the bedside in the intensive care setting on patientsfter aortic repair surgery for real-time monitoring of colon ischemiaith promising results.

ESULTS: In the first study, the cohort of colons monitored while

hey were being resected showed a significant decrease in glucose