The Beneficial Effect of HES on Vascular Permeability and Its Relationship With Endothelial Glycocalyx and Intercellular Junction After Hemorrhagic Shock

Abstract

Background: Vascular leakage is a common complication of hemorrhagic shock. Endothelial glycocalyx plays a crucial role in the protection of vascular endothelial barrier function. Hydroxyethyl starch (HES) is a commonly used resuscitation fluid for hemorrhagic shock. However, whether the protective effect of HES on vascular permeability after hemorrhagic shock is associated with the endothelial glycocalyx is unclear.Methods: Using hemorrhagic shock rat model and hypoxia treated vascular endothelial cells (VECs), effects of HES (130/0.4) on pulmonary vascular permeability and the relationship to endothelial glycocalyx were observed.Results: Pulmonary vascular permeability was significantly increased after hemorrhagic shock, as evidenced by the increased permeability of pulmonary vessels to albuminfluorescein isothiocyanate conjugate (FITC-BSA) and Evans blue, the decreased transendothelial electrical resistance of VECs and the increased transmittance of FITC-BSA. The structure of the endothelial glycocalyx was destroyed, showing a decrease in thickness. The expression of heparan sulfate, hyaluronic acid, and chondroitin sulfate, the components of the endothelial glycocalyx, was significantly decreased. HES (130/0.4) significantly improved the vascular barrier function, recovered the thickness and the expression of components of the endothelial glycocalyx by down-regulating the expression of heparinase, hyaluronidase, and neuraminidase, and meanwhile increased the expression of intercellular junction proteins ZO-1, occludin, and VE-cadherin. Degradation of endothelial glycocalyx with degrading enzyme (heparinase, hyaluronidase, and neuraminidase) abolished the beneficial effect of HES on vascular permeability, but had no significant effect on the recovery of the expression of endothelial intercellular junction proteins induced by HES (130/0.4). HES (130/0.4) decreased the expression of cleaved-caspase-3 induced by hemorrhagic shock.

Protective Effects of Dexmedetomidine on the Vascular Endothelial Barrier Function by Inhibiting Mitochondrial Fission via ER/Mitochondria Contact

“…Vascular endothelial cells were obtained from pulmonary veins of SD rats, as described previously ( Zhao et al, 2020 ). Rats were anesthetized and sterilized with iodine, and then rats received thoracotomy.…”

A narrative review of changes in microvascular permeability after burn

“…Findings from Zhao et al show that hydroxyethyl starch (130/0.4) has a protective effect on the vascular barrier function after hemorrhagic shock, and its mechanism is mainly related to the downregulation of heparinase, hyaluronidase, and neuraminic acid by hydroxyethyl starch. The expression of enzymes is related to the protective effect of endothelial glycocalyx and intercellular junction protein (27). In one study, Jacob et al injected physiological concentrations of type A, type B, and type C natriuretic peptides into the coronary arteries, and found that there were eluted glycocalyx components (proteoglycan-1 and heparan sulfate) in the coronary veins, the functional vascular barrier ability had been reduced, and that the formation of leakage and the exudation of colloidal hydroxyethyl starch had increased significantly.…”

Crystalloid and Colloid Compositions and Their Impact

“…Degree of volume expansion and longevity of HES, or any colloid, in plasma is difficult to predict. It will depend not only on the degree of vascular injury, but also on the MW and dispersity, amylase concentration, elimination rate into the urine, as well as its electrical charge, shape, and effect on the endothelial glycocalyx (31)(32)(33)(34)(35)(36)(37). Studies focusing on the immunologic, coagulation, and renal effects of HES products are not all in agreement, and species differences may exist (editor-See Article 7 Colloids, Yes or No?…”