CAJ | 학술논문

目的：探讨纳洛酮对右美托咪定麻醉小鼠有无催醒作用及其作用机制。方法30只清洁级昆明种小鼠随机分成纳洛酮组（NAL组）、阿替美唑组（ATI组）和生理盐水组（NS组）3组(n=10)。各组小鼠均腹腔注射右美托咪定1 mg/kg，给药后90 min，各组分别腹腔注射纳洛酮2 mg/kg、阿替美唑2 mg/kg与生理盐水10 mL/kg，于右美托咪定给药前及给药后5、15、30、60、90、95、105、120、180 min评估镇静、镇痛水平，并观察小鼠苏醒时间（以翻正反射恢复为标准）。结果各组在右美托咪定给药5 min后即表现明显的镇静、镇痛效应，约在60 min时达到峰效应和在180 min恢复；阿替美唑和纳洛酮均可降低右美托咪定的镇静、镇痛效应。NAL组在给药后95、105、120、180 min镇静评分均低于NS组，在95、105、120 min镇静评分均高于ATI组；NAL组在给药后95、105、120 min镇痛评分均低于NS组(均P＜0.05)，与ATI组差异均无统计学意义。ATI组、NAL组小鼠的苏醒时间短于NS组[min：(3.0±1.9) vs (5.0±2.5) vs (91.0±5.7)；F=1793.368，P＜0.05]，NAL组与ATI组差异无统计学意义。结论纳洛酮对右美托咪定麻醉小鼠具有一定的催醒作用。
목적：탐토납락동대우미탁미정마취소서유무최성작용급기작용궤제。방법30지청길급곤명충소서수궤분성납락동조（NAL조）、아체미서조（ATI조）화생리염수조（NS조）3조(n=10)。각조소서균복강주사우미탁미정1 mg/kg，급약후90 min，각조분별복강주사납락동2 mg/kg、아체미서2 mg/kg여생리염수10 mL/kg，우우미탁미정급약전급급약후5、15、30、60、90、95、105、120、180 min평고진정、진통수평，병관찰소서소성시간（이번정반사회복위표준）。결과각조재우미탁미정급약5 min후즉표현명현적진정、진통효응，약재60 min시체도봉효응화재180 min회복；아체미서화납락동균가강저우미탁미정적진정、진통효응。NAL조재급약후95、105、120、180 min진정평분균저우NS조，재95、105、120 min진정평분균고우ATI조；NAL조재급약후95、105、120 min진통평분균저우NS조(균P＜0.05)，여ATI조차이균무통계학의의。ATI조、NAL조소서적소성시간단우NS조[min：(3.0±1.9) vs (5.0±2.5) vs (91.0±5.7)；F=1793.368，P＜0.05]，NAL조여ATI조차이무통계학의의。결론납락동대우미탁미정마취소서구유일정적최성작용。
Objective To investigate the awaken effect of naloxon on dexmedetomidine anesthetized mice and its mechanism. Methods Thirty Kunming mice of clean grade were randomly divided into 3 groups which included NAL group (Naloxon group), ATI group(Atipamezole group)and NS group (Normal Saline group). All groups were given dexme?detomidine 1 mg·kg-1 intraperitoneally. Naloxon 2 mg·kg-1, atipamezole 2 mg·kg-1 and normal saline 10 mL·kg-1 were ran?domly given intraperitoneally to the NAL, ATI and NS group respectively 90 minutes after dexmedetomidine administration. At timepoints prior to dexmedetomidine administration and 5, 15, 30, 60, 90, 95, 105, 120, 180 minutes after it, the sedative and analgesic effects besides recovery time (based on restore of righting reflex loss) were assessed. Results Sedation and analgesia effects became apparent within 5 minutes, and peaked at approximately 60 minutes then spontaneously recovered at 180 minutes after injection of dexmedetomidine. The sedative and analgesic effects were reduced in both ATI and NAL groups. Compared with ATI group, the sedation scores were higher at 95, 105 and 120 minutes after dexmedetomidine admin?istration than those in NAL group (P<0.05) but the scores were not statistically significant at 180 minutes between these two groups. Compared with NS group, the sedation scores were lower at time points of 95, 105, 120 and 180 minutes than those in NAL group (P>0.05). The analgesic scores were not statistically significant at time points of 95, 105, 120 and 180 min?utes between NAL group and ATI group, but they were lower in NAL group compared with NS group at timepoints of 95, 105 and 120 minutes (P>0.05). The recovery time in ATI and NAL group were shorter than that in NS group (F=1 793.368, P<0.05), but it showed no statistical difference between ATI group and NAL group (P>0.05). Conclusion Naloxone had a certain awaken effect on dexmedetomidine anesthetized mice.