Glutamine preserves cardiomyocyte viability and enhances recovery of contractile function after ischemia-reperfusion injury.

Journal Article (Journal Article)

BACKGROUND: Glutamine has been shown to protect against cellular injury in in vitro gut epithelial cells and in vivo in the septic rat. Glutamine's effect on the cardiomyocyte has not been explored. We tested the hypothesis that glutamine can enhance heat shock protein 72 (HSP 72) expression, attenuate intracellular oxidant generation, and protect cardiomyocytes against ischemia/reperfusion (I/R) injury. METHODS: Chicken cardiomyocytes were supplemented with glutamine (10 mmol/L) or were controls (0 mmol/L). Cells underwent I/R, and HSP 72 content was evaluated using Western blotting. Reactive oxygen species generation was quantified through 2'-7'-dichlorofluorescin diacetate oxidation. Cell viability was quantified using propidium iodide staining. Return of contractile function was analyzed through phase contrast microscopy. RESULTS: Glutamine significantly increased cardiomyocyte HSP 72 expression and markedly reduced cell death after I/R injury. Glutamine did not significantly decrease intracellular oxidant generation. Contractile function returned in all glutamine-treated cells versus none of the control cells postreperfusion. CONCLUSIONS: Glutamine significantly increases cardiomyocytes survival and recovery of contractile function after I/R injury. This protection is associated with enhanced HSP 72 expression. These observations suggest that glutamine may prove beneficial as a protective therapy in patients at risk for cardiac ischemia and reperfusion injury, such as patients undergoing procedures requiring cardiopulmonary bypass and patients with coronary artery disease.

Full Text

Duke Authors

Cited Authors

  • Wischmeyer, PE; Vanden Hoek, TL; Li, C; Shao, Z; Ren, H; Riehm, J; Becker, LB

Published Date

  • 2003

Published In

Volume / Issue

  • 27 / 2

Start / End Page

  • 116 - 122

PubMed ID

  • 12665167

International Standard Serial Number (ISSN)

  • 0148-6071

Digital Object Identifier (DOI)

  • 10.1177/0148607103027002116


  • eng

Conference Location

  • United States