CAJ | 학술논문

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、6 h 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、6 h 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6 h 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、6 h MDA 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。
목적：탐토우미탁미정대대서지체결혈-재관주소치급성폐손상적영향급상관궤제。방법웅성청길급 SD 대서120지,수궤분위삼조：대조조、결혈-재관주조、우미탁미정조。재술전、지체결혈-재관주후0、1、3、6 h 측정대서 PaO2、폐조직습간비중(W/D)、혈청 SOD 활성、MDA 농도급 TNF-α수평,병관찰폐조직병이학변화。결과여대조조비교,결혈-재관주조재관주후0、1、3、6 h 폐조직 W/D 화 TNF-α수평명현승고(P <0.05),PaO2명현강저(P <0.05)；재관주1、3、6 h MDA농도명현승고(P <0.05),SOD 활성명현강저(P <0.05)。여결혈-재관주조비교,우미탁미정조재관주후6 h 폐조직 W/D 화 TNF-α명현하강、PaO2수평명현승고(P <0.05),재관주후3、6 h SOD 활성명현승고(P <0.05),재관주후1、3、6 h MDA 농도명현강저(P <0.05)。결론우미탁미정가이감경대서지체결혈-재관주소치적급성폐손상,기궤제여감경염성반응화항양화응격유관。
Objective To explore whether dexmedetomidine(Dex)could mitigate acute lung in-jury induced by hind limb ischemia reperfusion(I/R).Methods One hundred and twenty SD rat weigh-ting 250-300 g were allocated to receive hind limb I/R,I/R plus Dex (25 μg/kg Dex was intraperitoneal in-jection 30 min before ischemia)and norm control group,and each group was further divided into five sub-groups: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-αin the serum of the I/R 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 I/R plus group Dex.Conclusion Dex mitigates a-cute lung injury induced by unilateral hind limb I/R in rats.The mechanisms may involve attenuating oxida-tive stress and inhibiting inflammatory response.