Abstract
BackgroundOutcome in sepsis is mainly defined by the degree of organ failure, for which endothelial dysfunction at the macro- and microvascular level is an important determinant. In this study we evaluated endothelial function in patients with severe sepsis using cellular endothelial markers and in vivo assessment of reactive hyperaemia.Materials and MethodsPatients with severe sepsis (n = 30) and 15 age- and gender- matched healthy volunteers were included in this study. Using flow cytometry, CD34+/KDR+ endothelial progenitor cells (EPC), CD31+ T-cells, and CD31+/CD42b- endothelial microparticles (EMP) were enumerated. Migratory capacity of cultured circulating angiogenic cells (CAC) was assessed in vitro. Endothelial function was determined using peripheral arterial tonometry at the fingertip.ResultsIn patients with severe sepsis, a lower number of EPC, CD31+ T-cells and a decreased migratory capacity of CAC coincided with a blunted reactive hyperaemia response compared to healthy subjects. The number of EMP, on the other hand, did not differ. The presence of organ failure at admission (SOFA score) was inversely related with the number of CD31+ T-cells. Furthermore, the number of EPC at admission was decreased in patients with progressive organ failure within the first week.ConclusionIn patients with severe sepsis, in vivo measured endothelial dysfunction coincides with lower numbers and reduced function of circulating cells implicated in endothelial repair. Our results suggest that cellular markers of endothelial repair might be valuable in the assessment and evolution of organ dysfunction.
Highlights
Outcome in sepsis is mainly defined by the degree of organ failure, for which endothelial dysfunction at the macro- and microvascular level is an important determinant
In patients with severe sepsis, a lower number of endothelial progenitor cells (EPC), CD31+ T-cells and a decreased migratory capacity of circulating angiogenic cells (CAC) coincided with a blunted reactive hyperaemia response compared to healthy subjects
In patients with severe sepsis, in vivo measured endothelial dysfunction coincides with lower numbers and reduced function of circulating cells implicated in endothelial repair
Summary
Outcome in sepsis is mainly defined by the degree of organ failure, for which endothelial dysfunction at the macro- and microvascular level is an important determinant. In this study we evaluated endothelial function in patients with severe sepsis using cellular endothelial markers and in vivo assessment of reactive hyperaemia. Mortality and morbidity associated with sepsis are mainly determined by the development of organ dysfunction and degree of shock, in which macro- and microvascular dysfunction are key players [2,3]. Cellular mechanisms for endothelial repair, such as endothelial progenitor cells (EPC) and circulating angiogenic cells (CAC), are important for re-endothelialisation and neovascularisation [5,6,7]. As far as we know, data on the functional capacity of CAC in sepsis are scarce and confined to their proliferative capacity in vitro [9,11]
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