CAJ | 학술논문

目的：观察右美托咪定对大鼠布比卡因中枢神经系统（ CNS ）毒性的影响。方法 SD大鼠30只，随机分为3组，每组10只：布比卡因组（ B组）、右美托咪定5μg/kg ＋布比卡因组（ DB1组）、右美托咪定10μg/kg ＋布比卡因组（ DB2组）。 DB1，DB2组于输注布比卡因前10min 分别静脉输注右美托咪定5μg/kg，10μg/kg，B组输注等量0．9％氯化钠溶液，其后各组以2mg/（kg· min）速率静脉输注0．75％布比卡因，至大鼠出现惊厥时停药。持续监测平均动脉压（MAP）和心率（HR），于泵注布比卡因前、抽搐时采集动脉血进行血气分析，记录大鼠抽搐时布比卡因的用量。结果3组大鼠出现抽搐时的MAP均显著高于泵注布比卡因前（ P＜0．05），HR均显著慢于泵注布比卡因前（P＜0．05）。 B组大鼠出现惊厥时布比卡因用量为（5．6±1．2）mg/kg，与B组比较，DB1组、DB2组布比卡因用量[（7．7±1．4）mg/kg，（7．8±1．1mg/kg）]显著增大（P＜0．05），但DB1组和DB2组之间差异无显著性（P＞0．05）。结论预注右美托咪定可提高布比卡因诱发大鼠CNS毒性的阈值，减轻CNS毒性，但与右美托咪定剂量无关。
목적：관찰우미탁미정대대서포비잡인중추신경계통（ CNS ）독성적영향。방법 SD대서30지，수궤분위3조，매조10지：포비잡인조（ B조）、우미탁미정5μg/kg ＋포비잡인조（ DB1조）、우미탁미정10μg/kg ＋포비잡인조（ DB2조）。 DB1，DB2조우수주포비잡인전10min 분별정맥수주우미탁미정5μg/kg，10μg/kg，B조수주등량0．9％록화납용액，기후각조이2mg/（kg· min）속솔정맥수주0．75％포비잡인，지대서출현량궐시정약。지속감측평균동맥압（MAP）화심솔（HR），우빙주포비잡인전、추휵시채집동맥혈진행혈기분석，기록대서추휵시포비잡인적용량。결과3조대서출현추휵시적MAP균현저고우빙주포비잡인전（ P＜0．05），HR균현저만우빙주포비잡인전（P＜0．05）。 B조대서출현량궐시포비잡인용량위（5．6±1．2）mg/kg，여B조비교，DB1조、DB2조포비잡인용량[（7．7±1．4）mg/kg，（7．8±1．1mg/kg）]현저증대（P＜0．05），단DB1조화DB2조지간차이무현저성（P＞0．05）。결론예주우미탁미정가제고포비잡인유발대서CNS독성적역치，감경CNS독성，단여우미탁미정제량무관。
Objective To investigate the effects of dexmedetomidine pretreatment on bupivacaine associated toxicity to the central nervous system(CNS) in rats.Methods Thirty SD rats were randomly assigned to 3 groups(n=10 ):bupivacaine group ( B group ) , dexmedetomidine 5μg/kg+bupivacaine group ( DB1 group ) and dexmedetomidine 10μg/kg+bupivacaine group ( DB2 group ) .5μg/kg or 10μg/kg dexmedetomidine was given intravenously respectively in DB1 or DB2 group 10 min before bupivacaine infusion whereas equal volume of normal saline was injected instead in the B group.Rats in 3 groups received continuous infusion of bupivacaine at 2mg/(kg· min).Mean arterial pressure (MAP) and heart rate(HR) were monitored.Arterial blood was drawn before the beginning of local anesthetic infusion and at the onset of convulsions to determine blood gas tensions and pH .The amount of bupivacaine infused was ealculat-ed at the onset of convulsion .Results The MAP values were significantly increased and the HR was significantly de-creased at the onset of convulsion in all groups (P<0.05).In the DB1 and DB2 group,the amounts of bupivacaine cau-sing convulsion were(7.7 ±1.4)mg/kg,(7.8 ±1.1)mg/kg respectively,which were significantly higher than those in the B group(5.6 ±1.2mg/kg)(P<0.05).Conclusion Pretreatmaent with dexmedetomidine can raise the threshold for CNS toxicity and reduce toxicity induced by bupivacaine in rats ,whereas the effect is not dose-dependent .