中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2012年
3期
301-303
,共3页
斯妍娜%鲍红光%韩流%徐丽%王绪林%沈妍
斯妍娜%鮑紅光%韓流%徐麗%王緒林%瀋妍
사연나%포홍광%한류%서려%왕서림%침연
右美托咪啶%再灌注损伤%肾疾病
右美託咪啶%再灌註損傷%腎疾病
우미탁미정%재관주손상%신질병
Dexmedetomidine%Reperfusion injury%Kidney diseases
目的 评价右美托咪啶预先给药和后处理对大鼠肾缺血再灌注损伤的影响.方法 健康雄性Wistar大鼠32只,体重220~300 g,3~4月龄,采用随机数字表法,将大鼠随机分为4组(n=8):假手术组(S组)、缺血再灌注组(I/R组)、右美托咪啶预先给药组(Pre组)和右美托咪啶后处理组(Post组).肾缺血60min,再灌注48 h制备肾缺血再灌注损伤模型.Pre组和Post组分别于缺血前30 min和再灌注开始时腹腔注射右美托咪啶50μg/kg.于再灌注即刻、24、48 h(T1-3)时分别测定血清肌酐和血尿素的浓度.再灌注结束时取肾组织,光镜下观察病理学改变,并行急性肾小管坏死评分,采用TUNEL法测定细胞凋亡,计算细胞凋亡指数.结果 与S组比较,其余3组T2,3时血清肌酐和血尿素的浓度升高,急性肾小管坏死评分和细胞凋亡指数升高(P<0.05).与I/R组比较,Pre组和Post组T2,3时血清肌酐和血尿素浓度降低,急性肾小管坏死评分和细胞凋亡指数降低(P<0.05).结论 右美托咪啶预先给药和后处理均可减轻肾缺血再灌注损伤,其机制与抗细胞凋亡作用有关.
目的 評價右美託咪啶預先給藥和後處理對大鼠腎缺血再灌註損傷的影響.方法 健康雄性Wistar大鼠32隻,體重220~300 g,3~4月齡,採用隨機數字錶法,將大鼠隨機分為4組(n=8):假手術組(S組)、缺血再灌註組(I/R組)、右美託咪啶預先給藥組(Pre組)和右美託咪啶後處理組(Post組).腎缺血60min,再灌註48 h製備腎缺血再灌註損傷模型.Pre組和Post組分彆于缺血前30 min和再灌註開始時腹腔註射右美託咪啶50μg/kg.于再灌註即刻、24、48 h(T1-3)時分彆測定血清肌酐和血尿素的濃度.再灌註結束時取腎組織,光鏡下觀察病理學改變,併行急性腎小管壞死評分,採用TUNEL法測定細胞凋亡,計算細胞凋亡指數.結果 與S組比較,其餘3組T2,3時血清肌酐和血尿素的濃度升高,急性腎小管壞死評分和細胞凋亡指數升高(P<0.05).與I/R組比較,Pre組和Post組T2,3時血清肌酐和血尿素濃度降低,急性腎小管壞死評分和細胞凋亡指數降低(P<0.05).結論 右美託咪啶預先給藥和後處理均可減輕腎缺血再灌註損傷,其機製與抗細胞凋亡作用有關.
목적 평개우미탁미정예선급약화후처리대대서신결혈재관주손상적영향.방법 건강웅성Wistar대서32지,체중220~300 g,3~4월령,채용수궤수자표법,장대서수궤분위4조(n=8):가수술조(S조)、결혈재관주조(I/R조)、우미탁미정예선급약조(Pre조)화우미탁미정후처리조(Post조).신결혈60min,재관주48 h제비신결혈재관주손상모형.Pre조화Post조분별우결혈전30 min화재관주개시시복강주사우미탁미정50μg/kg.우재관주즉각、24、48 h(T1-3)시분별측정혈청기항화혈뇨소적농도.재관주결속시취신조직,광경하관찰병이학개변,병행급성신소관배사평분,채용TUNEL법측정세포조망,계산세포조망지수.결과 여S조비교,기여3조T2,3시혈청기항화혈뇨소적농도승고,급성신소관배사평분화세포조망지수승고(P<0.05).여I/R조비교,Pre조화Post조T2,3시혈청기항화혈뇨소농도강저,급성신소관배사평분화세포조망지수강저(P<0.05).결론 우미탁미정예선급약화후처리균가감경신결혈재관주손상,기궤제여항세포조망작용유관.
Objective To investigate the effects of dexmedctomidine pretreatment and postconditioning on renal ischemia-reperfusion (I/R) injury in rats.Methods Thirty-two male Wistar rats,aged 3-4 months,weighing 220-300 g,were randomly divided into 4 groups ( n =8 each):sham operation group ( group S),I/R group,dexmedetomidine pretreatment group (group Pre) and dexmedetomidine postconditioning group (group Post).The rats were anesthetized with phenobarbital sodium 65 mg/kg.Renal I/R was produced by occlusion of both renal pedicles for 60 min followed by 48 h reperfusion.Dexmedetomidine 50 μg/kg was given intraperitoneally at 30 min before ischemia and at the beginning of reperfusion in Pre and Post groups respectively.The concentrations of serum creatinine and blood urea were determined at 0,24 and 48 h of reperfusion (T1-3).The renal tissues were obtained at the end of reperfusion for microscopic examination and detection of apoptosis by TUNEL assay.Acute kidney tubular necrosis was scored and apoptosis index (AI) was calculated.Results Compared with group S,the concentration of serum creatinine and blood urea at T2.3,and acute kidney tubular necrosis score and AI were significantly increased in I/R,Pre and Post groups ( P < 0.05).Compared with I/R group,the concentration of serum creatinine and blood urea at T2.3,acute kidney tubular necrosis score and AI were significantly decreased in Pre and Post groups ( P < 0.05).Conclusion Both dexmedetomidine pretreatment and postconditioning can attenuate renal I/R injury through inhibition of cell apoptosis in rats.