CAJ | 학술논문

目的：探讨右美托咪定注射液（DEX）对大鼠心肺复苏（CPR）后氧化应激反应的保护作用及其机制。方法36只 SD 雄性大鼠随机分为3组，每组12只。假手术组（S 组），仅给予麻醉、气管插管和血管穿刺，不行窒息和心肺复苏；心肺复苏组（CPR 组）和右美托咪定干预组（DEX 组），均采用窒息法制备大鼠心搏骤停模型，行标准心肺复苏，待自主循环恢复（ROSC）后，DEX 组即刻给予 DEX 50μg/ kg 缓慢静脉注射，CPR 组即刻给予与 DEX 等量的生理盐水注射。分别在基础状态下及 ROSC 后3 h、12 h、24 h 抽取大鼠动脉血，并测定丙二醛（MDA）水平和超氧化物岐化酶（SOD）活性。结果 S 组大鼠均存活至24 h；CPR 组大鼠经复苏后有11只恢复自主循环，其中9只存活至24 h；DEX 组大鼠经复苏后有10只恢复自主循环，且均存活至24 h。3组大鼠在基础状态下 MDA 水平和 SOD 活性差异无显著性（ P ﹥0.05）。CPR 和 DEX 组大鼠复苏后其 MDA 水平逐渐增高，而 SOD 活性逐渐减低，均于12 h 达到最高（低）值。DEX 组大鼠在复苏后3 h、12 h、24 h 其 MDA 水平明显低于 CPR 组大鼠[3 h：（5.56±1.19）nmol/ ml 比（8.54±1.44）nmol/ ml，12 h：（8.13±1.93）nmol/ ml 比（13.60±2.97）nmol/ ml，24 h：（6.36±1.17）nmol/ ml 比（9.82±1.38）nmol/ ml]，差异均有统计学意义（均 P ﹤0.05）；DEX 组大鼠在复苏后3 h、12 h、24 h 其 SOD 活性明显高于 CPR 组大鼠[3 h：（152.50±13.59）U/ ml 比（135.09±12.97）U/ ml，12 h：（124.30±14.58）比（95.45±17.79）U/ ml，24 h：（132.50±11.61）比（106.63±9.34）U/ ml]，差异均有统计学意义（均 P ﹤0.05）。结论右美托咪定能够减轻大鼠心肺复苏后氧化应激反应，这一作用可能是通过抑制 MDA 产生、上调 SOD 活性实现的。
목적：탐토우미탁미정주사액（DEX）대대서심폐복소（CPR）후양화응격반응적보호작용급기궤제。방법36지 SD 웅성대서수궤분위3조，매조12지。가수술조（S 조），부급여마취、기관삽관화혈관천자，불행질식화심폐복소；심폐복소조（CPR 조）화우미탁미정간예조（DEX 조），균채용질식법제비대서심박취정모형，행표준심폐복소，대자주순배회복（ROSC）후，DEX 조즉각급여 DEX 50μg/ kg 완만정맥주사，CPR 조즉각급여여 DEX 등량적생리염수주사。분별재기출상태하급 ROSC 후3 h、12 h、24 h 추취대서동맥혈，병측정병이철（MDA）수평화초양화물기화매（SOD）활성。결과 S 조대서균존활지24 h；CPR 조대서경복소후유11지회복자주순배，기중9지존활지24 h；DEX 조대서경복소후유10지회복자주순배，차균존활지24 h。3조대서재기출상태하 MDA 수평화 SOD 활성차이무현저성（ P ﹥0.05）。CPR 화 DEX 조대서복소후기 MDA 수평축점증고，이 SOD 활성축점감저，균우12 h 체도최고（저）치。DEX 조대서재복소후3 h、12 h、24 h 기 MDA 수평명현저우 CPR 조대서[3 h：（5.56±1.19）nmol/ ml 비（8.54±1.44）nmol/ ml，12 h：（8.13±1.93）nmol/ ml 비（13.60±2.97）nmol/ ml，24 h：（6.36±1.17）nmol/ ml 비（9.82±1.38）nmol/ ml]，차이균유통계학의의（균 P ﹤0.05）；DEX 조대서재복소후3 h、12 h、24 h 기 SOD 활성명현고우 CPR 조대서[3 h：（152.50±13.59）U/ ml 비（135.09±12.97）U/ ml，12 h：（124.30±14.58）비（95.45±17.79）U/ ml，24 h：（132.50±11.61）비（106.63±9.34）U/ ml]，차이균유통계학의의（균 P ﹤0.05）。결론우미탁미정능구감경대서심폐복소후양화응격반응，저일작용가능시통과억제 MDA 산생、상조 SOD 활성실현적。
Objective To investigate the effects of dexmedetomidine(DEX)on improving systemic oxidative stress response after car-diopulmonary resuscitation(CPR)in rat model. Methods 36 male SD rats were randomly divided into sham operation group,CPR group and DEX group. In sham operation group,the rats underwent anesthesia,endotracheal intubation and vascular puncture without asphyxia and CPR. Rats cardiac arrest model were made with asphyxia and CPR was done in CPR group and DEX group. Rats of DEX group were injected 50 μg/ kg dexmedetomidine immediately after recovery of spontaneous circulation( ROSC). Rats of CPR group were injected saline using the same volume of DEX. Blood samples were taken before CPR and 3 h,12 h,24 h after ROSC. The levels of serum malondialdehyde(MDA)and superoxide dis-mutase(SOD)were detected respectively. Results Rats of sham operation group survived for 24 h. 11 rats recovered spontaneous circulation af-ter CPR and then 9 rats survived for 24 h in CPR group. 10 rats recovered spontaneous circulation after CPR and then survived for 24 h in DEX group. Baseline levels of MDA and SOD were respectively no significant difference among three groups. The levels of MDA decreased and reached bottom at 12 h later in CPR group and DEX group,and levels of SOD increased and reached peak at 12 h later in CPR group and DEX group after CPR. The levels of MDA in DEX group were significantly lower than those in CPR group since 3 h after ROSC[3 h(5. 56 ± 1. 19)vs.(8. 54 ± 1. 44)nmol/ ml;12 h:(8. 13 ± 1. 93)vs.(13. 60 ± 2. 97)nmol/ ml,24 h:(6. 36 ± 1. 17)vs.(9. 82 ± 1. 38)nmol/ ml](all P ﹤ 0. 05). The levels of SOD in DEX group were significantly higher than those in CPR group since 3 h after ROSC[(3 h:(152. 50 ± 13. 59)U/ ml vs.(135. 09 ± 12. 97)U/ ml,12 h:(124. 30 ± 14. 58)U/ ml vs.(95. 45 ± 17. 79)U/ ml,24 h:(132. 50 ± 11. 61)U/ ml vs.(106. 63 ± 9. 34)U/ ml] (all P ﹤ 0. 05). Conclusion DEX can reduce oxidative stress response after cardiopulmonary resuscitation in rat model,and this effect may be achieved by inhibiting the production of MDA and up regulation of SOD activity.