Effect of dexmedetomidine postconditioning on acute lung injury induced by lipopolysaccharide in rats / 中华麻醉学杂志

ABSTRACT

Objective To investigate the effect of dexmedetomidine postconditioning on acute lung injury (ALI) induced by lipopolysaccharide (LPS) in rats.Methods Fifty male Spragne-Dawley rats,aged 7-8 weeks,weighing 200-250 g,were randomly divided into 5 groups (n =10 each) using a random number tablecontrol group (group C),LPS group and postconditioning with 3 different doses of dexmedetomidine groups (LD,MD and HD groups).ALI was induced with LPS 8 mg/kg injected via the caudal vein in LPS,LD,MD and HD groups.Dexmedetomidine 5,10 and 15 μg/kg were injected intraperitoneally in LD,MD and HD groups,respectively,at 1 h after LPS injection.The equal volume of normal saline was injected intraperitoneally in C and L groups.Blood samples were taken from the left ventricle at 6 h after dexmedetomidine administration,then the animals were sacrificed and broncheoalveolar lavage fluid (BALF) was collected.The concentrations of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in plasma and BALF were detected by ELISA.The lungs were removed for microscopic examination of pathological changes and for determination of wet/dry lung weight (W/D) ratio and expression of Toll-like receptor 4 (TLR4) mRNA (by RT-PCR) in lung tissues.Results Compared with group C,W/D ratio,pathological scores,and the concentrations of IL-6 and TNF-α in plasma and BALF were significantly increased,and the expression of TLR4 mRNA was up-regulated in LPS,LD,MD and HD groups.Compared with LPS and LD groups,W/D ratio,pathological scores,and the concentrations of IL-6 and TNF-α in plasma and BALF were significantly decreased,and the expression of TLR4 mRNA was down-regulated in MD and HD groups.There was no significant difference in the parameters mentioned above between LPS and LD groups,and between MD and HD groups.Conclusion Dexmedetomidine postconditioning can alleviate ALI induced by LPS in rats,and up-regulated TLR4 mRNA expression and reduced inflammatory responses may be involved in the mechanism.