中文摘要：

目的评价右美托咪定对大鼠内毒素性脑损伤的影响。方法健康清洁级SD大鼠36只，6周龄，体重200～250g，采用随机数字表法，将其分为3组（n=12）：对照组（c组）、内毒素组（L组）和右美托咪定组（D组）。D组腹腔注射右美托咪定100μg／kg，15rain后股静脉注射LPS7．5mg／kg；L组腹腔注射等容量（2m1）生理盐水，15min后股静脉注射LPS7．5mg／kg；C组腹腔和股静脉注射2ml生理盐水。于LPS给药后2、4h时股动脉采血，ELISA法检测血清TNF—α浓度；LPS给药后12h，随机取6只大鼠股静脉注射伊文思蓝（EB）3ml／kg，1h后测定脑组织EB含量；另6只大鼠处死取脑组织，测定脑组织含水量，光镜下观察脑组织病理学结果。结果与C组比较，L组和D组脑组织含水量、EB含量和血清TNF-α浓度升高（P〈0．05）；与L组比较，D组上述指标均降低（P〈0．05）。D组脑组织病理学损伤程度轻于L组。结论右美托咪定可减轻大鼠内毒素性脑损伤，其机制可能与减轻脑组织炎性反应、改善血脑屏障通透性有关。

英文摘要：

Objective To investigate the effects of dexmedetomidine on lipopolysaccharide （LPS）-induced brain injury in rats. Methods Thirty-six pathogen-free Sprague-Dawley rats, aged 6 weeks, weighing 200-250 g, were randomly divided into 3 groups （n = 12 each） ： control group （group C）, LPS group （group L） and dexmedetomidine group （group D）. The animals were anesthetized with intraperitoneal 10% chloral hydrate 350 mg/kg, tracheostomized and mechanically ventilated. Dexmedetomidine 100 μg/kg was injected intraperitoneally and LPS 7.5 mg/kg was injected via the femoral vein 15 min later in group D. Normal saline 2 ml was injected intraperitoneally and LPS 7.5 mg/kg was injected via the femoral vein 15 min later in group L. Normal saline 2 ml was injected intraperitoneally and then injected via the femoral vein 15 min later in group C. Blood samples were obtained from the femoral artery at 2 and 4 h after LPS administration for determination of seium TNF-α concentration by ELISA. Six rats were chosen at 12 h after LPS administration, Evan＇s blue （EB） was injected via the femoral vein, and then the rats were sacrificed and brains removed for determination of EB content. Another six rats were sacrificed and their brains were immediately removed for determination of brain water content and for microscopic examination. Results The brain water content, EB content and serum TNF-α concentration were significantly increased in groups L and D as compared with group C （ P 〈 0.05）. The brain water content, EB content and serum TNF-α concentration were significantly lower in group D than in group L （ P 〈 0.05）. The microscopic examination showed that brain injury was attenuated in group D compared with group L. Conclusion Dexmedetomidine can reduce LPS-induced brain injury and reduction of the inflammatory response in the brain tissues and improvement in the permeability of the blood-brain barrier may be involved in the mechanism.