Blocking L-selectin function attenuates reperfusion injury following hemorrhagic shock in rabbits

Published

Journal Article

Leukocyte adhesion molecule (LAM) blockade reduces ischemia-reperfusion injury. We tested the hypothesis that a monoclonal antibody (MAb) that recognizes a functional epitope of L-selectin would decrease hemorrhagic shock-induced reperfusion injury. Anesthetized rabbits were subjected to 2 h of hemorrhagic shock (cardiac output reduced to 30% of baseline), then given one of the following treatments: MAbs that recognize functional domains of L- selectin (LAM1-3), CD18 (60.3), MAbs that recognize a nonfunctional domain on L-selectin (LAM1-14), or saline, immediately before resuscitation with shed blood. Additional fluids were administered as needed to maintain cardiac output at baseline levels for 6 h. The cumulative fluid resuscitation after MAb LAM1-3 (58 ± 34 ml/kg) was not significantly different from after MAb 60.3 (21 ± 24 ml/kg) or MAb LAM1-14 (66 ± 51 ml/kg), but it was significantly less than saline-treated controls (142 ± 142 ml/kg). However, two animals treated with MAb LAM1-14 died before 6 h. If their resuscitation volumes are projected to 6 h by linear regression, then the LAM1-14-treated group required significantly greater volume (101 ± 99 ml/kg) than the MAb LAM1-3-treated group. We conclude that MAbs to a functional domain on L- selectin are protective against reperfusion-injury following hemorrhagic shock.

Full Text

Duke Authors

Cited Authors

  • Ramamoorthy, C; Sharar, SR; Harlan, JM; Tedder, TF; Winn, RK

Published Date

  • January 1, 1996

Published In

Volume / Issue

  • 271 / 5 40-5

International Standard Serial Number (ISSN)

  • 0363-6135

Digital Object Identifier (DOI)

  • 10.1152/ajpheart.1996.271.5.h1871

Citation Source

  • Scopus