Acute hyperglycemia increases sepsis related glycocalyx degradation and endothelial cellular injury: A microfluidic study - 24/05/19
, David M. Liberati , Jonathan V. Martin Abstract |
Background |
Hyperglycemia promotes vascular inflammation; however its effect on endothelial dysfunction in sepsis is unknown. Microfluidic devices (MFD) may closely mimic the in vivo endothelial cell microenvironment. We hypothesized that stress glucose concentrations would increase sepsis related endothelial injury/activation.
Methods |
Human umbilical vein endothelial cell (HUVEC) monolayers were established in microfluidic channels. TNF was added followed by glucose. Endothelial glycocalyx (EG) integrity was indexed by shedding of the EG components as well as thickness. Endothelial cell (EC) injury/activation was indexed by soluble biomarkers. Intracellular reactive oxygen species (ROS) was by fluorescence.
Results |
TNF increased glycocalyx degradation and was associated with biomarkers of EC injury. These vascular barrier derangements were further increased by hyperglycemia. This may be related to increase ROS species generated followed by the combined insults.
Conclusion |
MFD technology may be a useful platform to study endothelial barrier function and stress conditions and allow preclinical assessment of potential therapies.
El texto completo de este artículo está disponible en PDF.Highlights |
• | Hyperglycemia in septic patients is common. Howvever its impact on outcomes is a subject of intense debate. |
• | Both sepsis and hyperglycemia cause endothelial dysfunction and degradation of the glycocalyx, which are key to the structural and functional integrity of the microcirculation. |
• | Stress concentrations of glucose were found to have an additive effect on sepsis induced vascular barrier injury in our model. This may be a therapeutic target to improve patient outcomes. |
Esquema
Vol 217 - N° 6
P. 1076-1082 - juin 2019 Regresar al número
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