ICAM-1 and VCAM-1 mediate endotoxemic myocardial dysfunction independent of neutrophil accumulation. American journal of physiology. Regulatory, integrative and comparative physiology [Am J Physiol Regul Integr Comp Physiol] Journal article

Title	ICAM-1 and VCAM-1 mediate endotoxemic myocardial dysfunction independent of neutrophil accumulation.
Author(s)	Raeburn CD, Calkins CM, Zimmerman MA, Song Y, Ao L, Banerjee A, Harken AH, Meng X
Institution	Department of Surgery, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA. christopher.raeburn@uchsc.edu
Source	Am J Physiol Regul Integr Comp Physiol 2002 Aug; 283(2):R477-86.
MeSH	Animals Antibodies Antineoplastic Agents, Phytogenic Cell Count Disease Models, Animal Disease Progression Endotoxemia Fluorescent Antibody Technique Heart Intercellular Adhesion Molecule-1 Lipopolysaccharides Male Mice Mice, Inbred C57BL Mice, Knockout Myocardium Neutrophil Infiltration Vascular Cell Adhesion Molecule-1 Vinblastine
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.
Language	eng
Pub Type(s)	In Vitro Journal Article Research Support, U.S. Gov't, P.H.S.
PubMed ID	12121861

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