| Summary: | Objective To investigate the protective effects of dexmedetomidine on endothelial barrier function in rats with sepsis. Methods 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 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 Dexmedetomidine can significantly improve the endothelial barrier function in rats with sepsis.
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