中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2014年
1期
68-71
,共4页
右美托咪啶%休克,脓毒性%一氧化氮合酶Ⅰ型%原癌基因蛋白质c-fos
右美託咪啶%休剋,膿毒性%一氧化氮閤酶Ⅰ型%原癌基因蛋白質c-fos
우미탁미정%휴극,농독성%일양화담합매Ⅰ형%원암기인단백질c-fos
Dexmedetomidine%Shock,septic%Nitric oxide synthase type Ⅰ%Proto-oncogene proteins c-fos
目的 评价右美托咪定对内毒素性休克大鼠蓝斑(LC)神经元型一氧化氮合酶(nNOS)和c-fos表达的影响.方法 选择雄性SD大鼠28只,8周龄,体重250 ～ 300 g,采用随机数字表法,将其分为4组(n=7):对照组(C组)、内毒素组(L组)、低剂量右美托咪定组(LD组)和高剂量右美托咪定组(HD组).C组和L组尾静脉注射生理盐水0.5 ml/kg,LD组和HD组分别尾静脉注射右美托咪定0.5和4.5μg/kg.10 min后,C组尾静脉注射生理盐水0.5 ml/kg,其余各组均尾静脉注射脂多糖5mg/kg.处死后取脑组织,测定脑组织含水量,采用免疫组织化学法测定LC区nNOS和c-fos阳性细胞数及其表达水平.结果 与C组比较,L组脑含水量升高,LC区nNOS和c-fos阳性细胞数明显增多,nNOS和c-fos表达上调(P＜0.05)；与L组比较,LD组和HD组脑含水量降低,LC区nNOS和c-fos阳性细胞数减少,nNOS和c-fos表达下调(P＜0.05)；与LD组比较,HD组LC区nNOS和c-fos阳性细胞数减少,nNOS和c-fos表达下调(P＜0.05).结论 右美托咪定可下调内毒素性休克大鼠LC区nNOS和c-fos表达,这可能是右美托咪定发挥脑保护作用的机制之一.
目的 評價右美託咪定對內毒素性休剋大鼠藍斑(LC)神經元型一氧化氮閤酶(nNOS)和c-fos錶達的影響.方法 選擇雄性SD大鼠28隻,8週齡,體重250 ～ 300 g,採用隨機數字錶法,將其分為4組(n=7):對照組(C組)、內毒素組(L組)、低劑量右美託咪定組(LD組)和高劑量右美託咪定組(HD組).C組和L組尾靜脈註射生理鹽水0.5 ml/kg,LD組和HD組分彆尾靜脈註射右美託咪定0.5和4.5μg/kg.10 min後,C組尾靜脈註射生理鹽水0.5 ml/kg,其餘各組均尾靜脈註射脂多糖5mg/kg.處死後取腦組織,測定腦組織含水量,採用免疫組織化學法測定LC區nNOS和c-fos暘性細胞數及其錶達水平.結果 與C組比較,L組腦含水量升高,LC區nNOS和c-fos暘性細胞數明顯增多,nNOS和c-fos錶達上調(P＜0.05)；與L組比較,LD組和HD組腦含水量降低,LC區nNOS和c-fos暘性細胞數減少,nNOS和c-fos錶達下調(P＜0.05)；與LD組比較,HD組LC區nNOS和c-fos暘性細胞數減少,nNOS和c-fos錶達下調(P＜0.05).結論 右美託咪定可下調內毒素性休剋大鼠LC區nNOS和c-fos錶達,這可能是右美託咪定髮揮腦保護作用的機製之一.
목적 평개우미탁미정대내독소성휴극대서람반(LC)신경원형일양화담합매(nNOS)화c-fos표체적영향.방법 선택웅성SD대서28지,8주령,체중250 ～ 300 g,채용수궤수자표법,장기분위4조(n=7):대조조(C조)、내독소조(L조)、저제량우미탁미정조(LD조)화고제량우미탁미정조(HD조).C조화L조미정맥주사생리염수0.5 ml/kg,LD조화HD조분별미정맥주사우미탁미정0.5화4.5μg/kg.10 min후,C조미정맥주사생리염수0.5 ml/kg,기여각조균미정맥주사지다당5mg/kg.처사후취뇌조직,측정뇌조직함수량,채용면역조직화학법측정LC구nNOS화c-fos양성세포수급기표체수평.결과 여C조비교,L조뇌함수량승고,LC구nNOS화c-fos양성세포수명현증다,nNOS화c-fos표체상조(P＜0.05)；여L조비교,LD조화HD조뇌함수량강저,LC구nNOS화c-fos양성세포수감소,nNOS화c-fos표체하조(P＜0.05)；여LD조비교,HD조LC구nNOS화c-fos양성세포수감소,nNOS화c-fos표체하조(P＜0.05).결론 우미탁미정가하조내독소성휴극대서LC구nNOS화c-fos표체,저가능시우미탁미정발휘뇌보호작용적궤제지일.
Objective To evaluate the effects of dexmedetomidine on the expression of neuronal nitric oxide synthase (nNOS) and c-fos in the lcuos cruleus (LC) in a rat model of endotoxic shock.Methods Twentyeight male Sprague-Dawley rats,aged 8 weeks,weighing 250-300 g,were randomly divided into 4 groups (n =7 each):control group (group C),endotoxic shock induced by lipopolysaccharide (LPS) group (group L),lowdose dexmedetomidine group (groupLD) and high-dose dexmedetomidine group (group HD).Normal saline 0.5 ml/kg was injected via the tail vein in C and L groups.Dexmedetomidine 0.5 and 4.5μg/kg were injected via the tail vein in group LD and group HD,respectively.Normal saline 0.5 ml/kg was injected via the tail vein 10 min later in C,while LPS 5 mg/kg was injected intravenously 10 min later in the other groups.The rats were sacrificed and their brains were removed for determination of brain water content,the number of nNOS and c-fos positive cells and expression of nNOS and c-fos in the LC by immuno-histochemistry.Results Compared with group C,the brain water content was significantly increased,the number of nNOS and c-fos positive cells in the LC was enlarged,and the expression of nNOS and c-fos in the LC was up-regulated in group L (P ＜ 0.05).The brain water content was significantly lower,the number of nNOS and c-fos positive cells in the LC was smaller,and the expression of nNOS and c-fos in the LC was lower in LD and HD groups than in group L (P ＜ 0.05).The number of nNOS and c-fos positive cells in the LC was significantly smaller,and the expression of nNOS and c-fos in the LC was lower in HD group than in group LD (P ＜ 0.05).Conclusion Dexmedetomidine can down-regulate the expression of nNOS and c-fos in the LC,which may be one of brain-protective mechanisms of dexmedetomidine in a rat model of endotoxic shock.
