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Cardiovascular Research 2006 72(1):134-142; doi:10.1016/j.cardiores.2006.06.029
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Copyright © 2006, European Society of Cardiology

Cardiac ICAM-1 mediates leukocyte-dependent decreased ventricular contractility in endotoxemic mice

Ehsan Y. Davani, John H. Boyd, Delbert R. Dorscheid, Yingjing Wang, Anna Meredith, Edmond Chau, Gurpreet K. Singhera and Keith R. Walley*

Critical Care Research Laboratories, St. Paul's Hospital, University of British Columbia, 1081 Burrard Street, Vancouver, BC, Canada V6Z 1Y6

* Corresponding author. Tel.: +1 604 806 8136; fax: +1 604 806 8351. Email address: kwalley{at}mrl.ubc.ca

Objective: Binding of ICAM-1 expressed on cardiomyocytes decreases cardiomyocyte contractility in vitro by altering the intracellular Ca2+ transient. We tested the hypothesis that signaling via ICAM-1 contributes to decreased left ventricular contractility in an in vivo model of systemic inflammation.

Methods: C57B6 wild-type mice and ICAM-1 knock-out mice were treated with intraperitoneal lipopolysaccharide (LPS) then left ventricular contractility was measured 6 h later using a volume-conductance micromanometer catheter. We repeated this experiment in chimeric mice lacking ICAM-1 expression in bone marrow-derived cells (M–) and/or lacking ICAM-1 expression in the heart and other tissues (H–).

Results: In C57B6 wild-type mice LPS injection significantly increased cardiac ICAM-1 expression and decreased in vivo measures of left ventricular contractility (end-systolic elastance, Ees decreased 58±4%, p<0.05, [dP/dtmax]/EDV decreased 60±6%, p<0.05). Cyclophosphamide pretreatment to decrease leukocyte count prevented the LPS-induced decrease in contractility. In ICAM-1 knock-out mice LPS did not decrease any measure of contractility. LPS did not decrease left ventricular contractility in M+/H– mice but decreased contractility in M+/H+ and M–/H+ mice to the same extent as in C57B6 wild-type mice implicating the importance of cardiac ICAM-1.

Conclusions: We conclude that signaling via cardiac ICAM-1 is necessary to mediate leukocyte-dependent decreases of left ventricular contractility in endotoxemic mice.

KEYWORDS Contractile function; Infection/inflammation; Leukocytes; Sepsis

* The support from Canadian Institutes of Health Research is acknowledged. K.R. Walley is a Michael Smith Foundation for Health Research distinguished scholar.

Time for primary review 21 days


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