Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 1993 Aug:(92):229-37.

Monoclonal antibodies to leukocyte and endothelial adhesion molecules attenuate ischemia-reperfusion injury

R K Winn  1 , D Mihelicic, N B Vedder, S R Sharar, J M Harlan
Affiliations
  • PMID: 8250813
Review

Monoclonal antibodies to leukocyte and endothelial adhesion molecules attenuate ischemia-reperfusion injury

R K Winn et al. Behring Inst Mitt. 1993 Aug.

Abstract

Neutrophils have been implicated as the cause of vascular injury that can lead to organ dysfunction and organ failure following a variety of initiating events. In particular, neutrophils have been shown to be necessary for vascular or tissue damage to occur in ischemia-reperfusion injuries of some organs and in the generalized ischemia-reperfusion injury resulting from hemorrhagic shock. Adherence of neurotrophils to endothelium or homotypic aggregation of neutrophils is thought to be necessary for injuries of this type to occur and these cell-cell interactions are mediated by adhesion molecules on both endothelial cells and leukocytes. In our completed studies, monoclonal antibodies that recognize functional epitopes of the leukocyte CD11/CD18 provided protection from ischemia-reperfusion injury. In addition, preliminary studies investigating leukocyte L-selectin and endothelial P-selectin appear to provide protection from ischemia-reperfusion injury.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

Publication types

MeSH terms

Substances

LinkOut - more resources