Abstract
Background
Studies have suggested a beneficial effect of early plasma-based resuscitation in
patients following trauma-hemorrhagic shock. The underlying mechanism(s) are unknown
but may be owing to protective effects of plasma components on the endothelium and
its glycocalyx layer. Albumin, the major protein in plasma, influences vascular integrity
and has antioxidant properties in vivo. Sphingosine 1-phosphate is a bioactive sphingolipid
with diverse signaling functions, which include endothelial barrier protection in
part owing to preservation of the glycocalyx. Sphingosine 1-phosphate is bound mainly
to albumin and high-density lipids in the plasma. Debate continues about the beneficial
effect of albumin solutions in shock resuscitation. Pharmacologic preparations may
modify constituents of albumin solutions for clinical use. We examined the relative
effects of sphingosine 1-phosphate concentrations in albumin solutions on the endothelial-glycocalyx
barrier in an in vitro microfluidic platform.
Methods
Endothelial cell monolayers were established in microfluidic perfusion devices and
exposed to control or biomimetic shock conditions followed by 5% plasma or different
albumin solutions ± exogenous sphingosine 1-phosphate perfusion. Biomarkers of endothelial
and glycocalyx activation, damage, and oxidant injury were then determined.
Results
Endothelial cell and glycocalyx barriers were damaged after biomimetic shock conditions.
Plasma and sphingosine 1-phosphate loaded albumin solutions protected against barrier
injury. Modest protective effects were noted with albumin alone; the efficacy varied
with sphingosine 1-phosphate content of the albumin solution.
Conclusion
The protective effect of albumin on the endothelia-glycocalyx barrier against oxidant
injury was dependent on its sphingosine 1-phosphate concentration. Our data may help
explain the discrepancies regarding the effectiveness of albumin solutions in shock
resuscitation.
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Article info
Publication history
Published online: November 11, 2022
Accepted:
August 4,
2022
Publication stage
In Press Corrected ProofIdentification
Copyright
© 2022 Elsevier Inc. All rights reserved.
