BACKGROUND: The vascular endothelium sustains substantial damage after severe insult. Recently, activated endothelial cells have been reported to produce microparticles in vitro. The objective of this study was to evaluate endothelial microparticle formation and microparticle-leukocyte interaction among patients with severe systemic inflammatory response syndrome (SIRS). METHODS: The participants in this study were 28 patients with severe SIRS (SIRS criteria and serum C-reactive protein > 10 mg/dL) and 18 healthy volunteers. Endothelial microparticles in the blood, microparticle-polymorphonuclear leukocyte (PMNL) binding, and PMNL oxidative activity were measured by flow cytometry. Soluble E-selectin, thrombomodulin, and plasminogen activator inhibitor-1 levels in the blood, variables representing systemic vascular endothelial cell activation and damage, and coagulative activity in the blood also were measured. RESULTS: Endothelial microparticle levels in the blood, microparticle binding to PMNLs, and oxidative activity in PMNLs increased significantly in patients with severe SIRS, as compared with the values in healthy volunteers. Soluble E-selectin, thrombomodulin, plasminogen activator inhibitor-1, and procoagulant activity in the blood also increased in these patients. CONCLUSIONS: Activated vascular endothelial cells with increased procoagulant activity enhance production of microparticles with increased binding to leukocytes in patients with severe SIRS. Endothelial microparticles may be involved in the pathogenesis of endothelial injury after severe insult.
BACKGROUND: The vascular endothelium sustains substantial damage after severe insult. Recently, activated endothelial cells have been reported to produce microparticles in vitro. The objective of this study was to evaluate endothelial microparticle formation and microparticle-leukocyte interaction among patients with severe systemic inflammatory response syndrome (SIRS). METHODS: The participants in this study were 28 patients with severe SIRS (SIRS criteria and serum C-reactive protein > 10 mg/dL) and 18 healthy volunteers. Endothelial microparticles in the blood, microparticle-polymorphonuclear leukocyte (PMNL) binding, and PMNL oxidative activity were measured by flow cytometry. Soluble E-selectin, thrombomodulin, and plasminogen activator inhibitor-1 levels in the blood, variables representing systemic vascular endothelial cell activation and damage, and coagulative activity in the blood also were measured. RESULTS: Endothelial microparticle levels in the blood, microparticle binding to PMNLs, and oxidative activity in PMNLs increased significantly in patients with severe SIRS, as compared with the values in healthy volunteers. Soluble E-selectin, thrombomodulin, plasminogen activator inhibitor-1, and procoagulant activity in the blood also increased in these patients. CONCLUSIONS: Activated vascular endothelial cells with increased procoagulant activity enhance production of microparticles with increased binding to leukocytes in patients with severe SIRS. Endothelial microparticles may be involved in the pathogenesis of endothelial injury after severe insult.
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