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Abnormal plasma microparticles impair vasoconstrictor responses in patients with cirrhosis

Pierre-Emmanuel Rautou1, Julie Bresson, Yannis Sainte-Marie

  • 1INSERM Unité 970, Paris Cardiovascular Research Center - PARCC, Paris, France.

Gastroenterology
|April 3, 2012
PubMed
Abstract

Insights

Patients with cirrhosis have increased circulating microparticles (MPs) from liver cells and leukocytes. These MPs impair blood vessel constriction, contributing to lower blood pressure and portal hypertension in advanced cirrhosis.

Area of Science:

  • Cardiovascular Biology
  • Hepatology
  • Immunology

Background:

  • Circulating membrane-shed microparticles (MPs) play a role in regulating vascular tone.
  • Portal hypertension in cirrhosis is associated with arterial vasodilation.
  • The cellular origins and vascular effects of MPs in cirrhosis are not fully understood.

Purpose of the Study:

  • To investigate the cellular origins of MPs in patients with cirrhosis.
  • To assess the contribution of these MPs to arterial vasodilation.
  • To determine the link between MPs and portal hypertension.

Main Methods:

  • Flow cytometry analysis of MPs in plasma from 91 cirrhosis patients and 30 controls.
  • In vitro and in vivo assessment of MP effects on vascular response to vasoconstrictors.
  • Analysis of MP subpopulations including endothelial, leukocyte, lymphocyte, erythrocyte, and hepatocyte-derived MPs.

Main Results:

  • Patients with cirrhosis exhibited higher levels of leuko-endothelial, pan-leukocyte, lymphocyte, and erythrocyte MPs compared to controls.
  • Hepatocyte-derived MPs were detected in cirrhosis patients but not in controls.
  • MPs from advanced cirrhosis patients impaired vascular contraction and decreased mean arterial blood pressure in mice, an effect dependent on cyclooxygenase type 1 and phosphatidylserine.

Conclusions:

  • Cirrhosis leads to increased circulating MPs, driven by systemic inflammation and liver cell damage.
  • The pool of MPs from advanced cirrhosis patients contributes to arterial vasodilation.
  • These MP-mediated vascular effects are implicated in the pathophysiology of portal hypertension.

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