Abstract
Objective To study the protective effects of hydrocortisone on glycocalyx in the vascular endothelium after trauma-hemorrhagic shock (T/HS) because the role of glycocalyx in maintaining the permeability of vascular endothelium intact, and in turn to identify the hydrocortisone protecting intestinal microcirculation. Methods Studies were carried out, in vivo, on a model of rats with induced T/HS. Intestinal perfusion and changes in endothelial glycocalyx and the associated molecular mechanism were assessed by using laser-Doppler velocimetry and electron microscopy, and the measurements of heparan sulfate, syndacan-1, and TNF-α in the superior mesenteric vein (SMV) with ELISA and Western-blot, and the expression of NF-κB in the vascular endothelium. Protective effects of hydrocortisone on the intestinal microcirculation after T/HS were evaluated. Results Degradation of the glycocalyx in intestinal vascular endothelium occurred 1 -3 hours after T/HS in rats (P <0.05) . By 3 hours later, significant reduction in intestinal perfusion was observed (P <0.05) . The level of TNF-α in the SMV and the expression of NF-κB in the vascular endothelium increased. With the use of hydrocortisone, intestinal perfusion was improved, and the degradation of glycocalyx was attenuated. Conclusions The degradation of glycocalyx is associated with the malfunction of intestinal microcirculation after T/HS. The NF-κB/TNF-α system in vascular endothelium participates in this process of glycocalyx degradation. Hydrocortisone may be a good agent to interrupt the course of glycocalx degradation. Key words: Traumatic hemorrhage shock; Capillary leak syndrome; Glycocalyx; Intestinal mucosal barrier; Hydrocortisone; TNF-α
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