The protective effects of hydrocortisone on glycocalyx in the intestinal capillary endothelium after trauma-hemorrhagic shock
10.3760/cma.j.issn.1671-0282.2015.05.006
- VernacularTitle:氢化可的松对创伤失血性休克后小肠血管内皮糖萼的保护作用
- Author:
Shunliang GAO
;
Jun ZHANG
;
Tingbo LIANG
- Publication Type:Journal Article
- Keywords:
Traumatic hemorrhage shock;
Capillary leak syndrome;
Glycocalyx;
Intestinal mucosal barrier;
Hydrocortisone;
TNF-α
- From:
Chinese Journal of Emergency Medicine
2015;24(5):481-487
- CountryChina
- Language:Chinese
-
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.
