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Related Experiment Videos

Statins (HMG-CoA reductase inhibitors) decrease postoperative adhesions by increasing peritoneal fibrinolytic

Cary B Aarons1, Philip A Cohen, Adam Gower

  • 1Department of Surgery, Boston University School of Medicine, Boston 02118, USA.

Annals of Surgery
|January 25, 2007
PubMed
Summary
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Statins administered intraperitoneally significantly reduced adhesion formation in rats by up-regulating tissue plasminogen activator (tPA) and decreasing plasminogen activator inhibitor-1 (PAI-1). This effect is mediated by cholesterol pathway intermediates affecting Rho protein signaling.

Area of Science:

  • Surgical research
  • Pharmacology
  • Cell biology

Background:

  • Intraperitoneal adhesions affect up to 95% of patients post-laparotomy.
  • Mechanisms that up-regulate peritoneal fibrinolysis reduce adhesion formation.
  • Statins are known to promote fibrinolysis in the cardiovascular system.

Purpose of the Study:

  • To determine if statins reduce adhesion formation in vivo.
  • To identify the mechanism of action of statins on adhesion formation in vitro.

Main Methods:

  • Adhesions were induced in rats using an ischemic button model.
  • Rats received vehicle, lovastatin, or atorvastatin intraperitoneally.
  • Tissue plasminogen activator (tPA) and plasminogen activator inhibitor-1 (PAI-1) levels were measured.

Related Experiment Videos

  • In vitro studies used human mesothelial cells (HMC) with cholesterol pathway intermediates.

    • Main Results:

    • Lovastatin and atorvastatin reduced adhesion formation by 26% and 58%, respectively.
    • Statins increased tPA levels and activity while PAI-1 levels remained unchanged.
    • In vitro, statins increased tPA and decreased PAI-1 production in HMC.
    • Cholesterol pathway intermediates reversed statin-induced changes, implicating Rho protein signaling.

    Conclusions:

    • Statins administered intraperitoneally can up-regulate local fibrinolysis.
    • In vitro studies suggest cholesterol pathway intermediates regulate Rho protein signaling, mediating statin effects.