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Related Experiment Videos

Hemodynamic forces regulate mural macrophage infiltration in experimental aortic aneurysms.

Eiketsu Sho1, Mien Sho, Katsuyuki Hoshina

  • 1Division of Vascular Surgery, Stanford University, Palo Alto, CA 94304, USA.

Experimental and Molecular Pathology
|March 11, 2004
PubMed
Summary

Altered blood flow and wall shear stress in abdominal aortic aneurysms (AAAs) impact macrophage behavior. Reduced blood flow decreases medial macrophage density, influencing AAA inflammation.

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Area of Science:

  • Cardiovascular Science
  • Biomedical Engineering
  • Inflammation Research

Background:

  • Abdominal aortic aneurysm (AAA) pathogenesis is influenced by blood flow (BF) and wall shear stress (WSS).
  • Oxidative stress and reactive oxygen species production are key factors in AAA disease.
  • Understanding hemodynamic influences on AAA inflammation is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the mechanisms by which hemodynamic forces modulate AAA inflammation.
  • To examine the effects of altered aortic flow on aneurysm macrophage density, chemotaxis, and survival.
  • To correlate gene expression of inflammatory mediators with macrophage infiltration under varying flow conditions.

Main Methods:

  • Rat abdominal aortic aneurysms (AAAs) were induced using porcine pancreatic elastase (PPE).

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  • Aneurysm blood flow was manipulated by creating arteriovenous fistulas (HF-AAA) or ligating the iliac artery (LF-AAA).
  • Macrophage density, apoptosis, and gene expression (MCP-1, GM-CSF) were quantified and correlated with WSS.

    • Main Results:

    • Wall shear stress (WSS) was significantly higher in high-flow AAAs (HF-AAA) compared to normal (NF-AAA) and low-flow (LF-AAA) conditions.
    • Reduced medial macrophage density and increased apoptosis were observed in LF-AAA, correlating with decreased WSS.
    • Adventitial macrophage density was not significantly affected by flow, but gene expression of MCP-1 and GM-CSF correlated with macrophage infiltration.

    Conclusions:

    • Luminal blood flow conditions play a regulatory role in AAA inflammation, primarily through modulation of medial macrophage density.
    • Hemodynamic forces, particularly WSS, may influence AAA progression and enlargement by regulating intimal macrophage behavior and survival.
    • These findings highlight the importance of hemodynamics in AAA pathophysiology and suggest potential therapeutic targets.