Shedding of the Endothelial Glycocalyx Independent of Systemic Tryptase Release during Oncologic Oral Surgery: An Observational Study.

Abstract

The endothelial glycocalyx and endothelial surface layer are crucial for several functions of the vasculature. Damage to the glycocalyx (“shedding”) occurs during diverse clinical conditions, including major surgery. Mast cell tryptase has been proposed as one possible “sheddase”. During oncologic oral surgery, glycocalyx shedding could be detrimental due to loss of vascular barrier function and consequent oedema in the musculocutaneous flap graft. Concentrations of the glycocalyx components heparan sulphate and syndecan-1, as well as of tryptase in blood serum before and after surgery, were measured in 16 patients undergoing oncologic oral surgery. Secondary measures were the concentrations of these substances on postoperative days 1 and 2. Heparan sulphate rose from 692 (median, interquartile range: 535–845) to 810 (638–963) ng/mL during surgery. Syndecan-1 increased from 35 (22–77) ng/mL to 138 (71–192) ng/mL. Tryptase remained virtually unchanged with 4.2 (3–5.6) before and 4.2 (2.5–5.5) ng/mL after surgery. Concentrations of heparan sulphate and syndecan-1 in serum increased during surgery, indicating glycocalyx shedding. Tryptase concentration remained equal, suggesting other sheddases than systemic tryptase release to be responsible for damage to the glycocalyx. Investigating strategies to protect the glycocalyx during oncologic oral surgery might hold potential to improve flap viability and patient outcome.