右美托咪定对犬体外循环后肺血管通透性的影响

目的探讨右美托咪定对犬体外循环（CPB）后肺血管通透性的影响。方法成年健康杂种犬54只，按随机数字表法分为对照组（C组）、CPB组（CPB组）和右美托咪定组（Dex组），每组18只。制备CPB诱发肺损伤模型，Dex组于CPB前即刻静脉泵注右美托眯啶1ug／（kg·min），随即予以1lag／（kg·h）持续泵注至实验结束；CPB组给予等量09％氯化钠溶液；C组不进行CPB，其余操作与CPB组相同。分别于CPB前（Tc）、CPB结束后30min（T1）、60min（T2）时采集动脉血样，测定呼吸指数（RI）、支气管肺泡灌洗液（BALF）中白细胞计数、总蛋白含量及TNF—a、IL-6浓度；测定肺组织伊文思蓝（EB）含量和肺湿／干质量比：光镜下观察肺组织病理学变化。结果与C组比较，CPB组和Dex组RI升高，BALF白细胞计数、总蛋白含量及TNF—a、IL-6浓度、EB含量和肺湿／干质量比升高（P〈0．05）；与CPB组比较，Dex组上述指标均降低（P〈0．05）；C组肺组织结构清晰，未见明显肺损伤；CPB组显示明显的肺部炎症反应，肺泡壁明显充血，肺泡隔增宽，Dex组病理学损伤程度较CPB组明显减轻。结论右美托咪定可明显降低CPB后肺血管通透性，其机制与减轻CPB后肺组织炎性反应有关。

Effects of dexmedetomidine on pulmonary vascular permeability of lung injury induced by cardiopulmonary bypass in dog YANG Xi- aoping,WANG Ying,QU Xianfeng,eta/. Department of Anesthesio/ogy,Taizhou Municipal Hospital,Taizhou 318000, China

Objective To assess the protective effect of dexmedetomidine on the pulmonary vascular permeability of the lung injury induced by cardiopulmonary bypass（CPB） in dogs. Methods Fifty four adult mongrel dogs weighted 15-16 kg, were divided into 3 groups （n=18 in each） randomly：control group （group C）, CPB group （group CPB） and dexmedetomidine group （group Dex）. The lung injury was induced by CPB in groups CPR and Dex; in group Dex 1 u g/kg dexmedetomidine was intra- venously injected immediately before CPB,followed by intravenous infusion at 1 # g/kg-h until the end of the experiment; in group CPB, the same volume of normal saline was injected. Blood samples were taken from the femoral artery before CPB （To）, 30 and 60 min after the termination of CPB（T, and T2）. Six animals were sacrificed at each time point. Respiratory index（RI） and the leu- cocyte count, albumin, TNF- a, IL-6 in bronchoalveolar lavage fiuid（BALF） were measured; Evan＇S blue（EB） content and the lung W/D weight ratio were determined subsequently. The pathological changes of lung tissues were observed with light microscopy. Results The RI, leucocyte count, albumin, TNF-a, IL-6 levels in BALF, EB content and the lung W/D weight ratio were signifi- cantly higher in groups CPB and Dex than those in group C. The above parameters in group Dex were significantly lower than those in group CPB. The pathological examination showed that lung injury was attenuated in group Dex compared with group CPB. Conclusion Dexmedetomidine can reduce pulmonary vascular permeability induced by CPB, which may be associated with the attenuation of inflammatory response in the lung tissues.