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Activated macrophages decrease rat cardiac myocyte contractility: importance of ICAM-1-dependent adhesion.

M G Simms1, K R Walley

  • 1University of British Columbia Pulmonary Research Laboratory, St. Paul's Hospital, Vancouver, British Columbia, Canada V6Z 1Y6.

The American Journal of Physiology
|July 17, 1999
PubMed
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Activated macrophages adhering to heart cells reduce their function. This cardiac dysfunction is mediated by intercellular adhesion molecule-1 (ICAM-1), tumor necrosis factor-alpha (TNF-alpha), free radicals, and nitric oxide.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Cellular Physiology

Background:

  • Macrophages are key immune cells involved in cardiac inflammatory responses.
  • Understanding macrophage interactions with cardiomyocytes is crucial for addressing myocardial dysfunction.

Purpose of the Study:

  • To investigate the direct impact of activated macrophages on cardiomyocyte contractile function.
  • To elucidate the molecular mechanisms underlying macrophage-induced myocardial dysfunction.

Main Methods:

  • Rat ventricular myocytes were co-cultured with elicited peritoneal macrophages.
  • Cardiac myocyte function (fractional shortening) was assessed using videomicroscopy under various inflammatory conditions.
  • Macrophage adherence to myocytes was quantified, and the role of ICAM-1 was examined using anti-ICAM-1 antibodies.

Related Experiment Videos

  • The involvement of TNF-alpha, oxygen free radicals, and nitric oxide was investigated using specific inhibitors and scavengers.

    • Main Results:

    • Direct contact between activated macrophages and cardiomyocytes significantly reduced myocyte fractional shortening.
    • Macrophage adherence to myocytes increased upon inflammatory challenge (TNF-alpha, endotoxin, IL-1beta) and correlated with decreased contractility.
    • Inhibition of ICAM-1, TNF-alpha, oxygen free radicals, or nitric oxide prevented the macrophage-induced decline in myocyte function.

    Conclusions:

    • Activated macrophages adhere to cardiomyocytes via ICAM-1, leading to impaired cardiac contractility.
    • The detrimental effects on cardiomyocyte function are mediated by TNF-alpha, oxygen free radicals, and nitric oxide.
    • Targeting macrophage-myocyte interactions presents a potential therapeutic strategy for inflammatory heart conditions.