Blockade of L-selectin attenuates reperfusion injury in a rat model.

Published

Journal Article

Ischemia/reperfusion (I/R) injury appears to be a significant neutrophil-dependent component and may be ameliorated by blocking leukocyte-endothelial adhesion. Using a rat extensor digitorum longus (EDL) muscle model, the present study tested the hypothesis that in vivo administration of the function-blocking monoclonal antibody (mAb) LAM1-116 which recognizes L-selectin, a cell-surface adhesion receptor, could decrease I/R injury. In 46 rats, one EDL served as a normal control and the opposite EDL underwent 3 hr of ischemia followed by 3 hr of reperfusion after pretreatment with LAM1-116 mAb, control IgG, or saline. Myeloperoxidase (MPO) activity showed only a two-fold increase from normal in LAM1-116-treated I/R EDL while a 27-fold increase occurred in the IgG2a and saline groups, with a statistically significant (p < 0.001) difference. A significantly (p < 0.05) lower wet weight ratio, improved fatigue contractile force, and less neutrophil infiltration were found in LAM1-116-treated EDL, when compared to those in control IgG- or saline-treated EDL. The results indicate that blockade of L-selectin by LAM1-116 mAb can effectively reduce neutrophil infiltration in reperfused skeletal muscle, thereby decreasing tissue edema and improving muscle fatigue contractile force. These findings may be important in understanding I/R injury.

Full Text

Duke Authors

Cited Authors

  • Yan, ZQ; Bolognesi, MP; Steeber, DA; Tedder, TF; Chen, LE; Seaber, AV; Urbaniak, JR

Published Date

  • April 2000

Published In

Volume / Issue

  • 16 / 3

Start / End Page

  • 227 - 233

PubMed ID

  • 10803628

Pubmed Central ID

  • 10803628

International Standard Serial Number (ISSN)

  • 0743-684X

Language

  • eng

Conference Location

  • United States