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ICAM-1 and VCAM-1 mediate endotoxemic myocardial dysfunction independent of neutrophil accumulation. Am J Physiol Regul Integr Comp Physiol 2002 Aug;283(2):R477-86

Date

07/18/2002

Pubmed ID

12121861

DOI

10.1152/ajpregu.00034.2002

Scopus ID

2-s2.0-0036333430   68 Citations

Abstract

Both intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) have been implicated in neutrophil-mediated lung and liver injury during sepsis. However, the role of these adhesion molecules as well as the contribution of neutrophils in myocardial dysfunction during sepsis remains to be determined. The purpose of this study was to examine the role of ICAM-1, VCAM-1, and neutrophils in lipopolysaccharide (LPS)-induced myocardial dysfunction. Mice were subjected to LPS (0.5 mg/kg ip) or vehicle (normal saline), and left ventricular developed pressure (LVDP) was determined by the Langendorff technique. LVDP was depressed by nearly 40% at 6 h after LPS. Immunofluorescent staining revealed a temporal increase in myocardial ICAM-1/VCAM-1 expression and neutrophils after LPS. Antibody blockade of VCAM-1 reduced myocardial neutrophil accumulation and abrogated LPS-induced cardiac dysfunction. Antibody blockade or absence of ICAM-1 (gene knockout) also abrogated LPS-induced cardiac dysfunction but did not reduce neutrophil accumulation. Neutrophil depletion (vinblastine or antibody) did not protect from LPS-induced myocardial dysfunction. Our results suggest that although endotoxemic myocardial dysfunction requires both ICAM-1 and VCAM-1, it occurs independent of neutrophil accumulation.

Author List

Raeburn CD, Calkins CM, Zimmerman MA, Song Y, Ao L, Banerjee A, Harken AH, Meng X

Authors

Casey Matthew Calkins MD Professor in the Surgery department at Medical College of Wisconsin
Michael A. Zimmerman MD, FACS Professor in the Surgery department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Animals
Antibodies
Antineoplastic Agents, Phytogenic
Cell Count
Disease Models, Animal
Disease Progression
Endotoxemia
Fluorescent Antibody Technique
Heart
In Vitro Techniques
Intercellular Adhesion Molecule-1
Lipopolysaccharides
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Myocardium
Neutrophil Infiltration
Vascular Cell Adhesion Molecule-1
Vinblastine
jenkins-FCD Prod-486 e3098984f26de787f5ecab75090d0a28e7f4f7c0