CAJ | 학술논문

目的评价右美托咪定对肾缺血再灌注诱发大鼠心肌损伤的影响.方法成年雄性Wistar大鼠24只,体重280 ～ 300 g,采用随机数字表法,将其分为3组(n=8):假手术组(S组)、肾缺血再灌注组(I/R组)、右美托咪定组(Dex组).S组仅游离双侧肾动脉,不结扎.I/R组用无创动脉夹结扎大鼠双侧肾动脉,缺血45 min后恢复灌注.Dex组于缺血前20 min腹腔注射右美托咪定50μg/kg,其余处理同I/R组.于再灌注24 h时取心肌组织,采用硫代巴比妥法测定心肌MDA含量,黄嘌呤氧化酶法测定SOD活性,采用流式细胞术检测心肌细胞凋亡情况,计算凋亡指数(AI),采用免疫组化法测定心肌Bcl-2及Bax的表达,计算Bcl-2/Bax比值.结果与S组相比,I/R组和Dex组AI和心肌MDA含量升高,SOD活性降低,I/R组Bcl-2/Bax比值降低,Dex组Bcl-2/Bax比值升高(P＜0.05);与 I/R组相比,Dex组AI和心肌MDA含量降低,SOD活性和Bcl-2/Bax比值升高(P＜0.05).结论右美托咪定可减轻肾缺血再灌注诱发大鼠心肌损伤,其机制可能与抑制心肌细胞凋亡和减轻脂质过氧化反应有关.
목적 평개우미탁미정대신결혈재관주유발대서심기손상적영향.방법 성년웅성Wistar대서24지,체중280 ～ 300 g,채용수궤수자표법,장기분위3조(n=8):가수술조(S조)、신결혈재관주조(I/R조)、우미탁미정조(Dex조).S조부유리쌍측신동맥,불결찰.I/R조용무창동맥협결찰대서쌍측신동맥,결혈45 min후회복관주.Dex조우결혈전20 min복강주사우미탁미정50μg/kg,기여처리동I/R조.우재관주24 h시취심기조직,채용류대파비타법측정심기MDA함량,황표령양화매법측정SOD활성,채용류식세포술검측심기세포조망정황,계산조망지수(AI),채용면역조화법측정심기Bcl-2급Bax적표체,계산Bcl-2/Bax비치.결과 여S조상비,I/R조화Dex조AI화심기MDA함량승고,SOD활성강저,I/R조Bcl-2/Bax비치강저,Dex조Bcl-2/Bax비치승고(P＜0.05);여 I/R조상비,Dex조AI화심기MDA함량강저,SOD활성화Bcl-2/Bax비치승고(P＜0.05).결론 우미탁미정가감경신결혈재관주유발대서심기손상,기궤제가능여억제심기세포조망화감경지질과양화반응유관.
Objective To evaluate the effect of dexmedetomidine on myocardial injury induced by renal ischemia-reperfusion (I/R) injury in rats.Methods Twenty-four male Wistar rats,weighing 280-300 g,were randomly divided into 3 groups (n =8 each):sham operation group (group S),group I/R and dexmedetomidine group (group Dex).Renal ischemia was induced by occlusion of bilateral renal arteries for 45 min followed by reperfusion in I/R and Dex groups.At 20 min before ischemia,dexmedetomidine 50 μg/kg was injected intraperitoneally in group Dex,and the rest procedures were similar to those previously described in group I/R.The rats were sacrificed at 24 h of reperfusion and myocardial specimens were obtained for determination of malondialdehyde (MDA) content and superoxide dismutase (SOD) activity.The apoptosis in cardiomyocytes was examined by flow cytometry.Apoptosis index was calculated.The expression of Bcl-2 and Bax was detected by immunohistochemistry,and Bcl-2/Bax ratio was calculated.Results Compared with group S,apoptosis index and MDA content were significantly increased in I/R and Dex groups,Bcl-2/Bax ratio was decreased in group I/R,and Bcl-2/Bax ratio was increased in group Dex.Compared with group I/R,apoptosis index and MDA content were significantly decreased,and SOD activity and Bcl-2/Bax ratio were increased in group Dex.Conclusion Dexmedetomidine can attenuate myocardial injury induced by renal I/R in rats,and the mechanism may be related to inhibited apoptosis in cardiomyocytes and reduced lipid peroxidation.