中华急诊医学杂志
中華急診醫學雜誌
중화급진의학잡지
CHINESE JOURNAL OF EMERGENCY MEDICINE
2015年
5期
481-487
,共7页
创伤失血性休克%毛细血管渗漏综合征%糖萼%肠道黏膜屏障%氢化可的松%肿瘤坏死因子-α
創傷失血性休剋%毛細血管滲漏綜閤徵%糖萼%腸道黏膜屏障%氫化可的鬆%腫瘤壞死因子-α
창상실혈성휴극%모세혈관삼루종합정%당악%장도점막병장%경화가적송%종류배사인자-α
Traumatic hemorrhage shock%Capillary leak syndrome%Glycocalyx%Intestinal mucosal barrier%Hydrocortisone%TNF-α
目的 糖萼作为血管内皮的“保护层”具有维持其通透性的作用,本研究期望证实创伤失血性休克能够导致肠道微循环内皮糖萼层的破坏,同时氢化可的松具有糖萼及肠道微循环的保护作用.方法 本研究以大鼠创伤失血性休克模型为基础,采用激光多普勒血流检测法观察小肠血流灌注,通过电镜直接观察及肠系膜上静脉内硫酸乙酰肝素(heparan sulfate)和多配体聚糖-1(syndecan-1)质量浓度检测评估内皮糖萼的破坏程度,分别采用ELISA及Western-blot法检测肠系膜上静脉TNF-α质量浓度及小肠内皮细胞NF-κB的表达,以探讨可能参与的分子机制,同时以氢化可的松治疗作为对照,评估其对创伤休克后小肠微循环功能的保护作用.结果 大鼠在发生休克后早期(3 h)即已出现肠道血流灌注显著下降(P＜0.05),小肠血管内皮糖萼的组成成分硫酸乙酰肝素和多配体聚糖-1在创伤休克早期发生大量降解(P＜0.01),同时电镜亦发现小肠微血管内皮糖萼层发生破坏变薄,氢化可的松的干预不仅缓解了糖萼的破坏,同时改善了创伤休克后小肠血流的灌注.创伤失血性休克后肠系膜上静脉血中TNF-α质量浓度较外周血显著升高,同时小肠内皮细胞NF-κB亦出现高表达,而氢化可的松的干预明显遏制了小肠内皮NF-κB的表达及TNF-α的产生.结论 创伤失血性休克可能导致了糖萼的破坏以及由此造成的小肠微循环障碍,内皮细胞NF-κB/TNF-α系统可能参与了糖萼的破坏的机制.以糖萼作为治疗靶点,氢化可的松可能具有较好的疗效.
目的 糖萼作為血管內皮的“保護層”具有維持其通透性的作用,本研究期望證實創傷失血性休剋能夠導緻腸道微循環內皮糖萼層的破壞,同時氫化可的鬆具有糖萼及腸道微循環的保護作用.方法 本研究以大鼠創傷失血性休剋模型為基礎,採用激光多普勒血流檢測法觀察小腸血流灌註,通過電鏡直接觀察及腸繫膜上靜脈內硫痠乙酰肝素(heparan sulfate)和多配體聚糖-1(syndecan-1)質量濃度檢測評估內皮糖萼的破壞程度,分彆採用ELISA及Western-blot法檢測腸繫膜上靜脈TNF-α質量濃度及小腸內皮細胞NF-κB的錶達,以探討可能參與的分子機製,同時以氫化可的鬆治療作為對照,評估其對創傷休剋後小腸微循環功能的保護作用.結果 大鼠在髮生休剋後早期(3 h)即已齣現腸道血流灌註顯著下降(P＜0.05),小腸血管內皮糖萼的組成成分硫痠乙酰肝素和多配體聚糖-1在創傷休剋早期髮生大量降解(P＜0.01),同時電鏡亦髮現小腸微血管內皮糖萼層髮生破壞變薄,氫化可的鬆的榦預不僅緩解瞭糖萼的破壞,同時改善瞭創傷休剋後小腸血流的灌註.創傷失血性休剋後腸繫膜上靜脈血中TNF-α質量濃度較外週血顯著升高,同時小腸內皮細胞NF-κB亦齣現高錶達,而氫化可的鬆的榦預明顯遏製瞭小腸內皮NF-κB的錶達及TNF-α的產生.結論 創傷失血性休剋可能導緻瞭糖萼的破壞以及由此造成的小腸微循環障礙,內皮細胞NF-κB/TNF-α繫統可能參與瞭糖萼的破壞的機製.以糖萼作為治療靶點,氫化可的鬆可能具有較好的療效.
목적 당악작위혈관내피적“보호층”구유유지기통투성적작용,본연구기망증실창상실혈성휴극능구도치장도미순배내피당악층적파배,동시경화가적송구유당악급장도미순배적보호작용.방법 본연구이대서창상실혈성휴극모형위기출,채용격광다보륵혈류검측법관찰소장혈류관주,통과전경직접관찰급장계막상정맥내류산을선간소(heparan sulfate)화다배체취당-1(syndecan-1)질량농도검측평고내피당악적파배정도,분별채용ELISA급Western-blot법검측장계막상정맥TNF-α질량농도급소장내피세포NF-κB적표체,이탐토가능삼여적분자궤제,동시이경화가적송치료작위대조,평고기대창상휴극후소장미순배공능적보호작용.결과 대서재발생휴극후조기(3 h)즉이출현장도혈류관주현저하강(P＜0.05),소장혈관내피당악적조성성분류산을선간소화다배체취당-1재창상휴극조기발생대량강해(P＜0.01),동시전경역발현소장미혈관내피당악층발생파배변박,경화가적송적간예불부완해료당악적파배,동시개선료창상휴극후소장혈류적관주.창상실혈성휴극후장계막상정맥혈중TNF-α질량농도교외주혈현저승고,동시소장내피세포NF-κB역출현고표체,이경화가적송적간예명현알제료소장내피NF-κB적표체급TNF-α적산생.결론 창상실혈성휴극가능도치료당악적파배이급유차조성적소장미순배장애,내피세포NF-κB/TNF-α계통가능삼여료당악적파배적궤제.이당악작위치료파점,경화가적송가능구유교호적료효.
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.
