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1.400042 重庆,陆军军医大学(第三军医大学)大坪医院:麻醉科
2.400042 重庆,陆军军医大学(第三军医大学)大坪医院:野战外科研究所战伤休克与输血研究室,创伤、烧伤与复合伤国家重点实验室
[胡弋, E-mail: huyi921@sina.com HU Yi, E-mail: huyi921@sina.com
收稿:2019-09-29,
修回:2019-12-09,
纸质出版:2020-02-28
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佘汉, 房贺, 李涛, 等. 右美托咪定对脓毒症大鼠血管内皮屏障功能的保护作用[J]. 第三军医大学学报, 2020,42(4):334-341.
Han SHE, He FANG, Tao LI, et al. Protective effect of dexmedetomidine on endothelial barrier function in rats with sepsis[J]. Journal of Third Military Medical University, 2020, 42(4): 334-341.
佘汉, 房贺, 李涛, 等. 右美托咪定对脓毒症大鼠血管内皮屏障功能的保护作用[J]. 第三军医大学学报, 2020,42(4):334-341. DOI: 10.16016/j.1000-5404.201909226.
Han SHE, He FANG, Tao LI, et al. Protective effect of dexmedetomidine on endothelial barrier function in rats with sepsis[J]. Journal of Third Military Medical University, 2020, 42(4): 334-341. DOI: 10.16016/j.1000-5404.201909226.
目的
2
探讨右美托咪定对脓毒症大鼠血管内皮屏障功能的保护作用。
方法
2
采用盲肠结扎穿孔(cecal ligation and puncture,CLP)诱导大鼠脓毒症模型,将SD大鼠分成4组:假手术(Sham)组、脓毒症(sepsis,Sep)组、常规治疗(conventional treatment,CT)组、右美托咪定(Dex)组,观察肠系膜微血管静脉通透性、肺血管通透性的变化及存活率、存活时间的变化;离体取原代肺静脉内皮细胞,观察右美托咪定对内毒素刺激血管内皮细胞后的闭锁小带蛋白1(zonula occludes-1,ZO-1)表达和细胞跨膜电阻(transmembrane electrical resistance,TER)的影响。
结果
2
与假手术组比较,脓毒症后大鼠肠系膜微血管和肺血管的通透性明显增加,存活率与存活时间明显降低(
P
<
0.01);常规治疗能够轻微降低脓毒症大鼠的血管通透性;右美托咪定可显著降低脓毒症大鼠肠系膜微血管和肺血管通透性(
P
<
0.01),提高脓毒症大鼠的存活率与存活时间(
P
<
0.05)。LPS孵育可导致肺静脉内皮细胞间连接断裂、消失,ZO-1表达明显降低,TER明显降低(
P
<
0.01)。
结论
2
右美托咪定可明显改善脓毒症大鼠的血管内皮屏障功能,并进一步发挥对脓毒症大鼠的保护作用。
Objective
2
To investigate the protective effects of dexmedetomidine on endothelial barrier function in rats with sepsis.
Methods
2
Sprague-Dawley rats were randomly divided into sham operation group
sepsis group
sepsis+conventional treatment group
and sepsis+dexmedetomidine group. In all but the sham operatioin group
the rats were subjected to cecal ligation and puncture (CLP) to induce sepsis and were given corresponding treatments. The vascular permeability of the mesenteric microvessels and the lungs was examined and the survival time and rate of the rats were recorded. In the cell experiment
the effect of dexmedetomidine on the expression of zonula occludes-1 (ZO-1) and transmembrane electrical resistance (TER) was observed in pulmonary vein endothelial cells stimulated with lipopolysaccharide (LPS).
Results
2
Compared with the sham-operated rats
the rats receiving CLP had significantly increased vascular permeability of the lungs and mesenteric microvessels with shortened survival time and a lowered survival rate (
P
<
0.01). Conventional treatment only slightly reduced the vascular permeability in rats with sepsis (
P
>
0.05). Dexmedetomidine treatment significantly decreased vascular permeability and increased the survival time and rate of the septic rats (
P
<
0.01). In the pulmonary vein endothelial cells
LPS stimulation significantly decreased the expression of ZO-1
caused obvious damage of the intercellular junctions and significantly reduced TER; these changes were significantly rescued by dexmedetomidine treatment.
Conclusion
2
Dexmedetomidine can significantly improve the endothelial barrier function in rats with sepsis.
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