内皮细胞微粒在休克复苏后血管渗漏中的作用及其与氧化应激的关系  

The role of endothelial deprived microparticle in regulation of vascular leakage and its relationship with oxidative stress during shock resuscitation

作　　者：张杰[1] 朱娱[1] 吴跃[1] 刘良明[1] 李涛[1] Zhang die;Zhu Yu;Wu Yue;Liu Liangming;Li Tao(State Key Laboratory of Trauma, Burns and Combined Injury, Department 2, Institute of Surgery Research, Daping Hospital, Third Military Medical University, Chongqing 400042, Chin)

机构地区：[1]第三军医大学大坪医院野战外科研究所第二研究室创伤、烧伤与复合伤国家重点实验室,重庆400042

出　　处：《中华实验外科杂志》2018年第7期1241-1243,共3页Chinese Journal of Experimental Surgery

基　　金：国家自然科学基金重点项目（81730059）;国家自然科学基金面上项目（81570441）

摘　　要：目的观察内皮微粒（EMP）在调节休克复苏大鼠血管渗漏中的作用及其与活性氧（ROS）的关系。方法利用休克复苏大鼠模型和缺氧复氧肺静脉内皮细胞，观察EMP含量与血管通透性变化的关系，ROS含量变化及对EMP含量和血管通透性的影响。结果休克复苏大鼠肺血管和缺氧复氧内皮细胞通透性显著升高（P=0．021），血浆EMP含量（P=0．009）和培养基中的EMP含量（P=0．003）显著升高；抑制EMP可显著降低休克复苏大鼠血管通透性（P=0．044）；缺氧复氧内皮细胞来源EMP显著升高正常大鼠血管通透性（P=0．028）。休克复苏大鼠静脉血管中ROS含量显著升高（P=0．007），ROS抑制剂可显著降低休克复苏大鼠血浆中的EMP含量（P=0．015）和血管通透性（P=0．046）；在细胞水平，缺氧复氧可显著升高内皮细胞中ROS、EMP含量（P=0．002）和单层内皮通透性（P=0．014）；ROS抑制剂可显著抑制缺氧复氧细胞EMP的产生（P=0．009）和通透性升高（P=0．023）；ROS激动剂显著升高内皮细胞通透性（P=0．019），而EMP抑制剂明显拮抗这种作用（P=0．024）。结论EMP在休克复苏血管渗漏中发挥重要作用，ROS可影响血浆EMP的含量变化。Objective To investigate the role of endothelial deprived microparticle （EMP） in regulation of vascular leakage and its relationship with oxidative （ROS） stress during shock resuscitation. Methods Hemorrhagic shock rats and pulmonary vein endothelial ceils were used to study the relationship between vascular permeability and EMP concentration and the effect of ROS inhibitor （ SS - 31 ） and agonist （H2 02 ） on EMP production and vascular permeability. Results The vascular permeability and the EMP production significantly increased during resuscitation （ P = 0. 021 ） , while inhibition of EMP production couht rescue the endothdial barrier function （P = 0. 044）. Intravenous administration of EMP increased the vascular permeability （P = 0. 028）. The ROS concentration in pulmonary vein increased during resuscitation （ P = 0. 007）. Inhibition of ROS by SS - 31 suppressed EMP production （P = 0. 015 ） and vascular permeability （P = 0. 046 ）. ROS agonist induced EMP production and increased vascular permeability （ P = 0. 019）, however this effect was abolished by EMP inhibitor （ P = 0. 024）. Conclusion EMP participates in regulation of vascular permeability during resuscitation, and ROS induced EMP production.

关 键 词：休克复苏 血管渗漏 内皮微粒 氧化应激 

分 类 号：R459.7[医药卫生—急诊医学]