Excess sodium is deleterious on endothelial and glycocalyx barrier function: A microfluidic study

Area of Science:

• Critical care medicine
• Endothelial biology
• Vascular physiology

Background:

• Hypernatremia is common in critically ill patients.
• High sodium may harm the vascular endothelial glycocalyx.
• The impact of hypernatremia on endothelial and glycocalyx barrier function requires investigation.

Purpose of the Study:

• To evaluate if high sodium concentration impairs endothelial and glycocalyx barrier function.
• To determine if shock conditions exacerbate hypernatremia's adverse effects on the glycocalyx.

Main Methods:

• Human umbilical vein endothelial cells (HUVEC) were cultured in microfluidic channels.
• Cells were exposed to high sodium concentrations (150 or 160 mEq/L).
• Simulated shock conditions (hypoxia/reoxygenation and epinephrine) were applied to subsets of cells.

Main Results:

• Hypernatremia caused glycocalyx degradation (hyaluronic acid, syndecan-1) and reduced thickness.
• Shock conditions exacerbated glycocalyx degradation and thickness reduction.
• Endothelial activation/injury markers (soluble thrombomodulin) and a profibrinolytic phenotype were observed.

Conclusions:

• Hypernatremia degrades the endothelial glycocalyx.
• Shock conditions worsen hypernatremia-induced glycocalyx damage.
• Further clinical studies are warranted to assess endothelial glycocalyx in hypernatremic patients.