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The Immune-Enhancing Enteral Agents Arginine and Glutamine Differentially Modulate Gut Barrier Function following Mesenteric Ischemia/Reperfusion

Kozar, Rosemary A. MD, PhD; Verner-Cole, Elizabeth BS; Schultz, Stanley G. MD; Sato, Nario MD; Bick, Roger J. PhD; DeSoignie, Roland MS; Poindexter, Brian J. MS; Moore, Frederick A. MD

Journal of Trauma and Acute Care Surgery: December 2004 - Volume 57 - Issue 6 - p 1150-1156
doi: 10.1097/01.TA.0000151273.01810.E9
Original Articles

Background: Immune-enhancing enteral diets have been shown to improve patient outcome. One contributing mechanism may be via maintenance of gut barrier function. While recent data has shown that glutamine is beneficial, arginine may be harmful. We therefore hypothesized that the immune-enhancing agents, glutamine and arginine, differentially modulate gut barrier function.

Methods: At laparotomy, rats had jejunal sacs filled with 10 mmol/L glutamine, arginine, fructose, or magnesium sulfate (osmotic control) followed by 60 minutes of superior mesenteric artery occlusion and 2 hours of reperfusion. Jejunum was harvested for histology, deconvolution microscopy, F:G actin, ATP, and permeability measurements.

Results: Glutamine and fructose minimized mucosal injury compared with controls and arginine. Deconvolution microscopy confirmed that glutamine and fructose preserved the actin cytoskeleton but there was disruption by arginine which correlated with F:G actin ratios and tissue ATP levels. Permeability was enhanced by arginine compared with the other groups.

Conclusion: Arginine resulted in worsened mucosal injury, disruption of the actin cytoskeleton, decreased tissue ATP and enhanced permeability compared with glutamine which appeared protective. The immune-enhancing agent arginine results in breakdown of gut barrier function which may have important implications for critically injured patients.

From the Departments of Surgery (R.A.K., E.V.-C., N.S., R.D., F.A.M.), Pathology (R.J.B., B.J.P.), and Integrative Biology and Pharmacology (S.G.S.) University of Texas-Houston, Houston, Texas.

Submitted for publication July 21, 2004.

Accepted for publication September 20, 2004.

Supported by NIGMS KO8 GM62975 (RAK).

Presented at the 34th Annual Meeting of the Western Trauma Association, February 22–27, 2004, Steamboat Springs, Colorado.

Address for reprints: Rosemary A. Kozar, MD, PhD, University of Texas-Houston, 6431 Fannin, MS 4.284 Houston, TX 77030; email:

© 2004 Lippincott Williams & Wilkins, Inc.