摘要
目的探讨右美托咪定对大鼠肢体缺血-再灌注所致急性肺损伤的影响及相关机制。方法雄性清洁级SD大鼠120只,随机分为三组:对照组、缺血-再灌注组、右美托咪定组。在术前、肢体缺血-再灌注后0、1、3、6h测定大鼠PaO2、肺组织湿干比重(W/D)、血清SOD活性、MDA浓度及TNF-α水平,并观察肺组织病理学变化。结果与对照组比较,缺血-再灌注组再灌注后0、1、3、6h肺组织W/D和TNF-α水平明显升高(P<0.05),PaO2明显降低(P<0.05);再灌注1、3、6 h MDA浓度明显升高(P<0.05),SOD活性明显降低(P<0.05)。与缺血-再灌注组比较,右美托咪定组再灌注后6h肺组织W/D和TNF-α明显下降、PaO2水平明显升高(P<0.05),再灌注后3、6 h SOD活性明显升高(P<0.05),再灌注后1、3、6hMDA浓度明显降低(P<0.05)。结论右美托咪定可以减轻大鼠肢体缺血-再灌注所致的急性肺损伤,其机制与减轻炎性反应和抗氧化应激有关。
Objective To explore whether dexmedetomidine（Dex） could mitigate acute lung injury induced by hind limb ischemia reperfusion（I/R）. Methods One hundred and twenty SD rat weighting 250-300 g were allocated to receive hind limb I/R, I/R plus Dex （25 μg/kg Dex was intraperitoneal injection 30 rain before iscbemia） and norm control group, and each group was further divided into five subgroups： before operation and 4 h ischemia followed by 0,1,3 and 6 h reperfusion. After euthanization, lung W/D weight ratio, PaO2 , SOD, MDA and TNF-α were determined. Results Compared with group C, hind limb I/R injury significantly increased serum TNF-α concentration and W/D ratio, with significantly decreasing PaO2 level at any time of reperfusion in the group I/R, the concentration of MDA increased and the SOD activity decresed at 1,3,6 h of reperfusion. Conversely, W/D ratio as well as the concentration of TNF-α in the serum of the UR plus group Dex were significantly lower than those of the I/R at 6 h of reperfusion, PaO2 level increased respectively; the concentration of MDA decresed at 1,3,6 h of reperfusion and the SOD activity increased at 3,6 h of reperfusion in UR plus group Dex. Conclusion Dex mitigates acute lung injury induced by unilateral hind limb I/R in rats. The mechanisms may involve attenuating oxidative stress and inhibiting inflammatory response.
出处
《临床麻醉学杂志》
CAS
CSCD
北大核心
2014年第6期602-605,共4页
Journal of Clinical Anesthesiology
