中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2011年
11期
1381-1383
,共3页
右美托咪啶%脑%再灌注损伤
右美託咪啶%腦%再灌註損傷
우미탁미정%뇌%재관주손상
Dexmedetomidine%Brain%Reperfusion injury
目的 评价右美托咪啶预先给药对大鼠局灶性脑缺血再灌注损伤的影响.方法 健康雄性SD大鼠100只,体重290～310 g,采用随机数字表法,将其随机分为5组(n=20):假手术组(SH组)、缺血再灌注组(I/R组)和不同剂量右美托咪啶预先给药组(L组、M组和H组).I/R组、L组、M组和H组采用线栓法建立大鼠局灶性脑缺血再灌注损伤模型,缺血60 min后行再灌注.L组、M组和H组于缺血前15 min分别腹腔注射右美托咪啶100、200和400 μg/kg,I/R组腹腔注射等容量生理盐水.再灌注24h时,随机取10只大鼠,测定神经功能缺陷评分和脑梗死体积,观察脑组织病理学改变；随机取10只大鼠,测定缺血侧脑组织热休克蛋白70(HSP70)表达、Na+ -K+ -ATP酶活性和血浆SOD活性、皮质醇浓度.结果 与SH组比较,I/R组、L组、M组和H组神经功能缺陷评分和皮质醇浓度升高,SOD和Na+ -K+ -ATP酶的活性降低,HSP70表达上调(P＜0.05)；与I/R组比较,L组、M组和H组神经功能缺陷评分、脑梗死体积和皮质醇浓度降低,HSP70表达上调,SOD和Na+ -K+ -ATP酶的活性升高,且呈剂量依赖性(P＜0.05),病理学损伤程度呈剂量依赖性减轻.结论 右美托咪啶预先给药可减轻大鼠局灶性脑缺血再灌注损伤,且呈剂量依赖性,其机制可能与改善脑细胞能量代谢、减轻脂质过氧化反应和应激反应有关.
目的 評價右美託咪啶預先給藥對大鼠跼竈性腦缺血再灌註損傷的影響.方法 健康雄性SD大鼠100隻,體重290～310 g,採用隨機數字錶法,將其隨機分為5組(n=20):假手術組(SH組)、缺血再灌註組(I/R組)和不同劑量右美託咪啶預先給藥組(L組、M組和H組).I/R組、L組、M組和H組採用線栓法建立大鼠跼竈性腦缺血再灌註損傷模型,缺血60 min後行再灌註.L組、M組和H組于缺血前15 min分彆腹腔註射右美託咪啶100、200和400 μg/kg,I/R組腹腔註射等容量生理鹽水.再灌註24h時,隨機取10隻大鼠,測定神經功能缺陷評分和腦梗死體積,觀察腦組織病理學改變；隨機取10隻大鼠,測定缺血側腦組織熱休剋蛋白70(HSP70)錶達、Na+ -K+ -ATP酶活性和血漿SOD活性、皮質醇濃度.結果 與SH組比較,I/R組、L組、M組和H組神經功能缺陷評分和皮質醇濃度升高,SOD和Na+ -K+ -ATP酶的活性降低,HSP70錶達上調(P＜0.05)；與I/R組比較,L組、M組和H組神經功能缺陷評分、腦梗死體積和皮質醇濃度降低,HSP70錶達上調,SOD和Na+ -K+ -ATP酶的活性升高,且呈劑量依賴性(P＜0.05),病理學損傷程度呈劑量依賴性減輕.結論 右美託咪啶預先給藥可減輕大鼠跼竈性腦缺血再灌註損傷,且呈劑量依賴性,其機製可能與改善腦細胞能量代謝、減輕脂質過氧化反應和應激反應有關.
목적 평개우미탁미정예선급약대대서국조성뇌결혈재관주손상적영향.방법 건강웅성SD대서100지,체중290～310 g,채용수궤수자표법,장기수궤분위5조(n=20):가수술조(SH조)、결혈재관주조(I/R조)화불동제량우미탁미정예선급약조(L조、M조화H조).I/R조、L조、M조화H조채용선전법건립대서국조성뇌결혈재관주손상모형,결혈60 min후행재관주.L조、M조화H조우결혈전15 min분별복강주사우미탁미정100、200화400 μg/kg,I/R조복강주사등용량생리염수.재관주24h시,수궤취10지대서,측정신경공능결함평분화뇌경사체적,관찰뇌조직병이학개변；수궤취10지대서,측정결혈측뇌조직열휴극단백70(HSP70)표체、Na+ -K+ -ATP매활성화혈장SOD활성、피질순농도.결과 여SH조비교,I/R조、L조、M조화H조신경공능결함평분화피질순농도승고,SOD화Na+ -K+ -ATP매적활성강저,HSP70표체상조(P＜0.05)；여I/R조비교,L조、M조화H조신경공능결함평분、뇌경사체적화피질순농도강저,HSP70표체상조,SOD화Na+ -K+ -ATP매적활성승고,차정제량의뢰성(P＜0.05),병이학손상정도정제량의뢰성감경.결론 우미탁미정예선급약가감경대서국조성뇌결혈재관주손상,차정제량의뢰성,기궤제가능여개선뇌세포능량대사、감경지질과양화반응화응격반응유관.
Objective To investigate the effect of dexmedetomidine pretreatment on focal cerebral ischemia-reperfusion(I/R) injury in rats.Methods One hundred male SD rats weighing 290-310 g were randomly divided into 5 groups(n =20 each):sham operation group(group SH) ; focal cerebral I/R group; focal cerebral I/R + dexmedetomidine 100 μg/kg(group L); focal cerebral I/R+ dexmedetomidine 200 μg/kg (group M) and focal cerebral I/R + dexmedetomidine 400 μg/kg(group H).Focal cerebral I/R was produced by occlusion of middle cerebral artery for 60 min followed by 24 h of reperfusion.Dexmedetomidine 100,200 and 400 μg/kg were injected intraperitoneally 15 min before ischemia in groups L,M and H respectively.While equal volume of normal saline was injected intraperitoneally in group SH.Neurologic function was assessed and scored at 24 h of reperfusion.Then the animals were sacrificed and brains were removed for determination of cerebral infarct volume and microscopic examination.The expression of heat shock protein 70(HSP70) and activity of Na+ -K + -ATPase in ischemic cortex and activity of SOD and concentration of cortisol in plasma were determinationed at 24 h of reperfusion.Results Compared with group SH,neurologic deficit scores and plasma concentration of cortisol were significantly increased,activities of SOD and Na+ -K+ -ATPase decreased and expression of HSP70 was up-regulated in groups I/R,L,M and H( P ＜ 0.05).Compared with group I/R,neurologic deficit scores and plasma concentration of cortisol were significantly decreased,activities of SOD and Na+ -K+ -ATPase increased and expression of HSP70 was up-regulated in a dose-dependent manner ( P ＜ 0.05),and the pathological change was reduced in a dose-dependent manner in groups L,M and H.Conclusion Dexmedetomidine pretreatment can attenuate focal cerebral I/R injury in a dose-dependent manner through improvement of brain cell energy metabolism and reduction of lipid peroxidation and stress reaction.
