中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2015年
5期
546-549
,共4页
张军%杨红梅%谢淑华%王雷%耿立成
張軍%楊紅梅%謝淑華%王雷%耿立成
장군%양홍매%사숙화%왕뢰%경립성
麻醉药,吸入%二异丙酚%淀粉样β蛋白%海马%认知%老年人
痳醉藥,吸入%二異丙酚%澱粉樣β蛋白%海馬%認知%老年人
마취약,흡입%이이병분%정분양β단백%해마%인지%노년인
Anesthetics,inhalation%Propofol%Amyloid beta-protein%Hippocampus%Cognition%Aged
目的：评价异丙酚和七氟醚麻醉对老龄小鼠认知功能和海马β淀粉样蛋白（Aβ）沉积的影响。方法 SAMP8小鼠36只，6月龄，体重29～32 g，采用随机数字表法，将其分为4组（ n＝9）：正常对照组（C组）、异丙酚麻醉组（P 组）、七氟醚麻醉组（S组）和异丙酚复合七氟醚麻醉组（PS组）。 P组腹腔注射异丙酚140 mg∕kg，首次出现翻正反射时追加异丙酚70 mg∕kg，再次出现时追加异丙酚40 mg∕kg；S组持续吸入2％七氟醚120 min；PS组腹腔注射异丙酚80 mg∕kg后持续吸入1％七氟醚120 min，出现翻正反射时追加异丙酚40 mg∕kg，3组均维持麻醉约120 min。分别于麻醉前及麻醉后7、14、28 d时进行Morris水迷宫实验，记录逃避潜伏期，然后取海马，采用免疫组化法检测Aβ表达。结果与C组比较，S组麻醉后7 d时逃避潜伏期延长，麻醉后7、14、28 d时海马Aβ表达上调（P＜0．05），P组和PS组上述指标差异无统计学意义（P＞0．05）；与麻醉后7 d时比较，S组麻醉后14、28 d时海马Aβ表达下调，C组、P组和PS组各时点海马Aβ表达差异无统计学意义（ P＞0．05）。结论七氟醚麻醉虽然可促进老龄小鼠海马Aβ沉积，但是仅导致短期认知功能障碍，而异丙酚及异丙酚复合七氟醚麻醉对其均无影响。
目的：評價異丙酚和七氟醚痳醉對老齡小鼠認知功能和海馬β澱粉樣蛋白（Aβ）沉積的影響。方法 SAMP8小鼠36隻，6月齡，體重29～32 g，採用隨機數字錶法，將其分為4組（ n＝9）：正常對照組（C組）、異丙酚痳醉組（P 組）、七氟醚痳醉組（S組）和異丙酚複閤七氟醚痳醉組（PS組）。 P組腹腔註射異丙酚140 mg∕kg，首次齣現翻正反射時追加異丙酚70 mg∕kg，再次齣現時追加異丙酚40 mg∕kg；S組持續吸入2％七氟醚120 min；PS組腹腔註射異丙酚80 mg∕kg後持續吸入1％七氟醚120 min，齣現翻正反射時追加異丙酚40 mg∕kg，3組均維持痳醉約120 min。分彆于痳醉前及痳醉後7、14、28 d時進行Morris水迷宮實驗，記錄逃避潛伏期，然後取海馬，採用免疫組化法檢測Aβ錶達。結果與C組比較，S組痳醉後7 d時逃避潛伏期延長，痳醉後7、14、28 d時海馬Aβ錶達上調（P＜0．05），P組和PS組上述指標差異無統計學意義（P＞0．05）；與痳醉後7 d時比較，S組痳醉後14、28 d時海馬Aβ錶達下調，C組、P組和PS組各時點海馬Aβ錶達差異無統計學意義（ P＞0．05）。結論七氟醚痳醉雖然可促進老齡小鼠海馬Aβ沉積，但是僅導緻短期認知功能障礙，而異丙酚及異丙酚複閤七氟醚痳醉對其均無影響。
목적：평개이병분화칠불미마취대노령소서인지공능화해마β정분양단백（Aβ）침적적영향。방법 SAMP8소서36지，6월령，체중29～32 g，채용수궤수자표법，장기분위4조（ n＝9）：정상대조조（C조）、이병분마취조（P 조）、칠불미마취조（S조）화이병분복합칠불미마취조（PS조）。 P조복강주사이병분140 mg∕kg，수차출현번정반사시추가이병분70 mg∕kg，재차출현시추가이병분40 mg∕kg；S조지속흡입2％칠불미120 min；PS조복강주사이병분80 mg∕kg후지속흡입1％칠불미120 min，출현번정반사시추가이병분40 mg∕kg，3조균유지마취약120 min。분별우마취전급마취후7、14、28 d시진행Morris수미궁실험，기록도피잠복기，연후취해마，채용면역조화법검측Aβ표체。결과여C조비교，S조마취후7 d시도피잠복기연장，마취후7、14、28 d시해마Aβ표체상조（P＜0．05），P조화PS조상술지표차이무통계학의의（P＞0．05）；여마취후7 d시비교，S조마취후14、28 d시해마Aβ표체하조，C조、P조화PS조각시점해마Aβ표체차이무통계학의의（ P＞0．05）。결론칠불미마취수연가촉진노령소서해마Aβ침적，단시부도치단기인지공능장애，이이병분급이병분복합칠불미마취대기균무영향。
Objective To evaluate the effects of propofol and sevoflurane anesthesia on cognitive function and amyloid beta protein ( Aβ) deposition in hippocampi of aged mice. Methods Thirty?six SAMP8 mice, aged 6 months, weighing 29-32 g, were randomly assigned into 4 groups ( n=9 each) using a random number table: control group ( group C ) , propofol anesthesia group ( group P ) , sevoflurane anesthesia group (group S) and propofol plus sevoflurane anesthesia group (group PS). In group P, propofol 140 mg∕kg was injected intraperitoneally, when righting reflex occurred, additional propofol 70 mg∕kg was given, and when it occurred again, additional propofol 40 mg∕kg was given. Group S continuously inhaled 1% sevoflurane for 120 min. Group PS continuously inhaled 2% sevoflurane for 120 min, and when righting reflex occurred, additional propofol 40 mg∕kg was given. Anesthesia was maintained for 120 min in P, S and PS groups. Before anesthesia and at 7, 14 and 28 days after anesthesia, Morris water maze test was performed, and the escape latency was recorded. Hippocampi were obtained to determine the expression of Aβ using immuno?histochemistry. Results Compared with group C, the escape latency was significantly prolonged at 7 days after anesthesia, and the expression of Aβwas up?regulated at 7, 14 and 28 days after anesthesia in group S, and no significant change was found in the parameters mentioned above in P and PS groups. Compared with the value at 7 days after anesthesia, the expression of Aβ was significantly down?regulated at 14 and 28 days after anesthesia in group S, and no significant change was found in the expression of Aβ at 14 and 28 days after anesthesia in C, P and PS groups. Conclusion Although sevoflurane anesthesia promotes Aβ deposition in hippocampi, it only causes short?term cognitive dysfunction, however, anesthesia with propofol or with propofol in combination with sevoflurane produces no influence in aged mice.
