中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2015年
4期
423-425
,共3页
刘祥%霍树平%王亮%何金华%袁天宝%王秀丽%王秋筠
劉祥%霍樹平%王亮%何金華%袁天寶%王秀麗%王鞦筠
류상%곽수평%왕량%하금화%원천보%왕수려%왕추균
卡配因%麻醉药,吸入%麻醉%老年人%细胞凋亡
卡配因%痳醉藥,吸入%痳醉%老年人%細胞凋亡
잡배인%마취약,흡입%마취%노년인%세포조망
Calpain%Anesthetics,inhalation%Anesthesia%Aged%Apoptosis
目的 评价钙蛋白酶在七氟醚麻醉诱发老龄大鼠海马神经元凋亡中的作用.方法 健康雌性SD大鼠54只,18月龄,体重450~ 550 g,采用随机数字表法,将其分为3组(n=18):对照组(C组)、七氟醚组(Sev组)和钙蛋白酶抑制剂MDL28170组(M组).C组吸入50%O2-50%N2混合气体3 h;Sev组吸入3%七氟醚3 h;M组尾静脉注射MDL28170 10 mg/kg,30 min后吸入3%七氟醚3h,同时尾静脉输注MDL28170 3.33 mg·kg-1·h-1.每组取9只大鼠,分别于麻醉前30 min和麻醉后1~5d时采用Morris水迷宫实验评价认知功能,记录逃避潜伏期和穿越原平台次数;分别于麻醉前30 min和麻醉后1、5d水迷宫测试结束后,每组处死3只大鼠,取海马组织,采用流式细胞术测定神经元凋亡率和胞浆钙离子浓度.结果 与C组比较,Sev组和M组麻醉后1d时逃避潜伏期延长,穿越原平台次数减少,神经元凋亡率和胞浆钙离子浓度升高(P<0.05);与Sev组比较,M组麻醉后1d时逃避潜伏期缩短,穿越原平台次数增多,神经元凋亡率降低(P<0.05),胞浆钙离子浓度差异无统计学意义(P>0.05).结论 钙蛋白酶激活参与了七氟醚麻醉诱发老龄大鼠海马神经元凋亡.
目的 評價鈣蛋白酶在七氟醚痳醉誘髮老齡大鼠海馬神經元凋亡中的作用.方法 健康雌性SD大鼠54隻,18月齡,體重450~ 550 g,採用隨機數字錶法,將其分為3組(n=18):對照組(C組)、七氟醚組(Sev組)和鈣蛋白酶抑製劑MDL28170組(M組).C組吸入50%O2-50%N2混閤氣體3 h;Sev組吸入3%七氟醚3 h;M組尾靜脈註射MDL28170 10 mg/kg,30 min後吸入3%七氟醚3h,同時尾靜脈輸註MDL28170 3.33 mg·kg-1·h-1.每組取9隻大鼠,分彆于痳醉前30 min和痳醉後1~5d時採用Morris水迷宮實驗評價認知功能,記錄逃避潛伏期和穿越原平檯次數;分彆于痳醉前30 min和痳醉後1、5d水迷宮測試結束後,每組處死3隻大鼠,取海馬組織,採用流式細胞術測定神經元凋亡率和胞漿鈣離子濃度.結果 與C組比較,Sev組和M組痳醉後1d時逃避潛伏期延長,穿越原平檯次數減少,神經元凋亡率和胞漿鈣離子濃度升高(P<0.05);與Sev組比較,M組痳醉後1d時逃避潛伏期縮短,穿越原平檯次數增多,神經元凋亡率降低(P<0.05),胞漿鈣離子濃度差異無統計學意義(P>0.05).結論 鈣蛋白酶激活參與瞭七氟醚痳醉誘髮老齡大鼠海馬神經元凋亡.
목적 평개개단백매재칠불미마취유발노령대서해마신경원조망중적작용.방법 건강자성SD대서54지,18월령,체중450~ 550 g,채용수궤수자표법,장기분위3조(n=18):대조조(C조)、칠불미조(Sev조)화개단백매억제제MDL28170조(M조).C조흡입50%O2-50%N2혼합기체3 h;Sev조흡입3%칠불미3 h;M조미정맥주사MDL28170 10 mg/kg,30 min후흡입3%칠불미3h,동시미정맥수주MDL28170 3.33 mg·kg-1·h-1.매조취9지대서,분별우마취전30 min화마취후1~5d시채용Morris수미궁실험평개인지공능,기록도피잠복기화천월원평태차수;분별우마취전30 min화마취후1、5d수미궁측시결속후,매조처사3지대서,취해마조직,채용류식세포술측정신경원조망솔화포장개리자농도.결과 여C조비교,Sev조화M조마취후1d시도피잠복기연장,천월원평태차수감소,신경원조망솔화포장개리자농도승고(P<0.05);여Sev조비교,M조마취후1d시도피잠복기축단,천월원평태차수증다,신경원조망솔강저(P<0.05),포장개리자농도차이무통계학의의(P>0.05).결론 개단백매격활삼여료칠불미마취유발노령대서해마신경원조망.
Objective To evaluate the role of calpain in sevoflurane anesthesia-induced apoptosis in hippocampal neurons of aged rats.Methods Fifty-four healthy female Sprague-Dawley rats,aged 18 months,weighing 450-550 g,were randomly divided into 3 groups (n=12 each) using a random number table:control group (group C),sevoflurane group (Sev group) and calpain inhibitor M DL28170 group (group M).In group C,the rats inhaled 50% O2-50%N2 for 3 h.In Sev group,the rats inhaled 3% sevoflurane for 3 h.In group M,MDL28170 10 mg/kg was injected via the tail vein,30 min later 3% sevoflurane was inhaled for 3 h,and MDL28170 was simultaneously infused at 3.33 mg · kg 1 · h-1 via the tail vein.Nine rats in each group were selected,and cognitive function was assessed by using Morris water maze test at 30 min before anesthesia and 1-5 days after anesthesia.The escape latency and frequency of crossing the original platform were recorded.After the end of Morris water maze test performed at 30 min before anesthesia and 1-5 days after anesthesia,3 rats in each group were sacrificed,and hippocampal tissues were obtained for detection of cell apoptosis (by flow cytometry) and intracellular [Ca2+] i.Apoptotic rate was calculated.Results Compared with group C,the escape latency was significantly prolonged,and the frequency of crossing the original platform was decreased,and the apoptotic rate and intracellular [Ca2+]i were increased at 1 day after anesthesia in Sev and M groups.Compared with group Sev,the escape latency was significantly shortened,the frequency of crossing the original platform was increased,and the apoptotic rate was decreased at 1 day after anesthesia,and no significant change was found in intracellular [Ca2+]i in group M.Conclusion Calpain activation is involved in sevoflurane anesthesia-induced apoptosis in hippocampal neurons of aged rats.