中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2015年
1期
111-113
,共3页
熊颖芬%吕艳霞%金小雪%孟叶%谢明明
熊穎芬%呂豔霞%金小雪%孟葉%謝明明
웅영분%려염하%금소설%맹협%사명명
哌啶类%再灌注损伤%肾%蛋白激酶C
哌啶類%再灌註損傷%腎%蛋白激酶C
고정류%재관주손상%신%단백격매C
Piperidines%Reperfusion injury%Kidney%Protein kinase C
目的 探讨瑞芬太尼对大鼠肾缺血再灌注时蛋白激酶C(PKC)活性的影响.方法 清洁级健康成年雄性SD大鼠75只,体重250～ 300 g,采用随机数字表法,将其分为5组(n=15):假手术组(S组)、缺血再灌注组(I/R组)、瑞芬太尼组(R组)、纳洛酮组(N组)和纳洛酮+瑞芬太尼组(NR组).采用夹闭双侧肾动脉45 min恢复灌注的方法制备大鼠肾缺血再灌注损伤模型.R组和NR组于缺血前15 min时尾静脉输注瑞芬太尼1.0 μg·kg-1 ·min-1,持续输注90 min;N组和NR组于缺血前20 min时及缺血35 min时尾静脉注射纳洛酮0.3 mg/kg.于再灌注24 h时处死大鼠,取肾组织,透射电镜下观察肾小管上皮细胞超微结构,采用ELISA法确定肾组织PKC活性,采用免疫组化法测定肾组织PKC表达.结果 与S组比较,其余4组肾组织PKC活性升高,R组肾组织PKC表达上调(P＜0.01);与I/R组比较,R组肾组织PKC活性升高,PKC表达上调(P＜0.01),病理学损伤减轻;与R组比较,N组和NR组肾组织PKC活性降低,PKC表达下调(P＜0.01),病理学损伤加重.结论 瑞芬太尼减轻大鼠肾缺血再灌注损伤的机制可能与其通过激活阿片受体,上调PKC表达,升高PKC活性有关.
目的 探討瑞芬太尼對大鼠腎缺血再灌註時蛋白激酶C(PKC)活性的影響.方法 清潔級健康成年雄性SD大鼠75隻,體重250～ 300 g,採用隨機數字錶法,將其分為5組(n=15):假手術組(S組)、缺血再灌註組(I/R組)、瑞芬太尼組(R組)、納洛酮組(N組)和納洛酮+瑞芬太尼組(NR組).採用夾閉雙側腎動脈45 min恢複灌註的方法製備大鼠腎缺血再灌註損傷模型.R組和NR組于缺血前15 min時尾靜脈輸註瑞芬太尼1.0 μg·kg-1 ·min-1,持續輸註90 min;N組和NR組于缺血前20 min時及缺血35 min時尾靜脈註射納洛酮0.3 mg/kg.于再灌註24 h時處死大鼠,取腎組織,透射電鏡下觀察腎小管上皮細胞超微結構,採用ELISA法確定腎組織PKC活性,採用免疫組化法測定腎組織PKC錶達.結果 與S組比較,其餘4組腎組織PKC活性升高,R組腎組織PKC錶達上調(P＜0.01);與I/R組比較,R組腎組織PKC活性升高,PKC錶達上調(P＜0.01),病理學損傷減輕;與R組比較,N組和NR組腎組織PKC活性降低,PKC錶達下調(P＜0.01),病理學損傷加重.結論 瑞芬太尼減輕大鼠腎缺血再灌註損傷的機製可能與其通過激活阿片受體,上調PKC錶達,升高PKC活性有關.
목적 탐토서분태니대대서신결혈재관주시단백격매C(PKC)활성적영향.방법 청길급건강성년웅성SD대서75지,체중250～ 300 g,채용수궤수자표법,장기분위5조(n=15):가수술조(S조)、결혈재관주조(I/R조)、서분태니조(R조)、납락동조(N조)화납락동+서분태니조(NR조).채용협폐쌍측신동맥45 min회복관주적방법제비대서신결혈재관주손상모형.R조화NR조우결혈전15 min시미정맥수주서분태니1.0 μg·kg-1 ·min-1,지속수주90 min;N조화NR조우결혈전20 min시급결혈35 min시미정맥주사납락동0.3 mg/kg.우재관주24 h시처사대서,취신조직,투사전경하관찰신소관상피세포초미결구,채용ELISA법학정신조직PKC활성,채용면역조화법측정신조직PKC표체.결과 여S조비교,기여4조신조직PKC활성승고,R조신조직PKC표체상조(P＜0.01);여I/R조비교,R조신조직PKC활성승고,PKC표체상조(P＜0.01),병이학손상감경;여R조비교,N조화NR조신조직PKC활성강저,PKC표체하조(P＜0.01),병이학손상가중.결론 서분태니감경대서신결혈재관주손상적궤제가능여기통과격활아편수체,상조PKC표체,승고PKC활성유관.
Objective To investigate the effect of remifentanil on protein kinase C (PKC) activity during renal ischemia-reperfusion (I/R) in rats.Methods Seventy-five male Sprague-Dawley rats,weighing 250-300 g,were randomly divided into 5 groups (n=15 each) using a random number table:sham operation group (group S),I/R group,remifentanil group (group R),naloxone group (group N),and naloxone + remifentanil group (group NR).Renal ischemia was induced by clamping the bilateral renal arteries for 45 min using an atraumatic clamp followed by reperfusion.In R and NR groups,remifentanil 1.0 μg · kg-1 · min-1was infused via the caudal vein starting from 15 min before ischemia until 30 min of reperfusion.In N and NR groups,naloxone 0.3 mg/kg was injected via the caudal vein at 20 min before ischemia and 35 min of ischemia,respectively.The rats were sacrificed at 24 h of reperfusion and the kidneys were removed for determination of the ultrastructure of the renal tubular epithelial cells (using transmission electron microscope),activity of PKC in renal tissues (by ELISA),and expression of the PKC in renal tissues (by immuno-histochemistry).Results Compared with group S,the activity of PKC in renal tissues was significantly increased in the other four groups,and the expression of the PKC in renal tissues was up-regulated in group R.Compared with group I/R,the activity of PKC in renal tissues was significantlyincreased,the expression of PKC in renal tissues was up-regulated,and the pathological changes were attenuated in group R.Compared with group R,the activity of PKC in renal tissues was significantly decreased,the expression of PKC in renal tissues was down-regulated,and the pathological changes were aggravated in N and NR groups.Conclusion The mechanism by which remifentanil attenuates renal I/R injury may be related to up-regulation of PKC expression and increase in PKC activity through activating opioid receptors in rats.
