中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2010年
11期
1364-1366
,共3页
哌啶类%心肌再灌注损伤%NF-κB
哌啶類%心肌再灌註損傷%NF-κB
고정류%심기재관주손상%NF-κB
Piperidines%Myocardial reperfusion injury%NF-kappa B
目的 探讨瑞芬太尼对兔心肌缺血再灌注时NF-κB活性的影响.方法 健康成年新西兰大白兔50只,月龄2～3月,体重2.0～2.5 kg,随机分为5组(n=10):假手术组(S组)左冠状动脉前降支只穿线不结扎;缺血再灌注组(IR组)冠状动脉前降支穿线结扎30 min,再灌注120 min;S组和IR组在缺血前10 min时颈外静脉输注生理盐水5 ml·kg-1·h-1至再灌注120 min;低、中、高剂量瑞芬太尼组(L组、M组、H组)缺血前10 min时颈外静脉输注瑞芬太尼1、5、10μg·kg-1·min-1至再灌注120 min,余处理同IR组.再灌注120 min时处死动物取心脏,采用Western blot法测定心肌细胞核NF-κB的表达水平,以反映其活性,观察心肌组织病理学结果.结果 与S组比较,其余各组NF-κB活性升高(P＜0.05);与IR组比较,L组、M组和H组NF-κB活性降低(P＜0.05),L组、M组和H组NF-κ:B活性依次降低(P＜0.05);病理学结果显示:L组、M组和H组心肌缺血再灌注损伤程度较IR组减轻,且随剂量增加,损伤逐渐减轻.结论 静脉输注瑞芬太尼可通过降低NF-κB活性减轻兔心肌缺血再灌注损伤,其效应呈剂量依赖性.
目的 探討瑞芬太尼對兔心肌缺血再灌註時NF-κB活性的影響.方法 健康成年新西蘭大白兔50隻,月齡2～3月,體重2.0～2.5 kg,隨機分為5組(n=10):假手術組(S組)左冠狀動脈前降支隻穿線不結扎;缺血再灌註組(IR組)冠狀動脈前降支穿線結扎30 min,再灌註120 min;S組和IR組在缺血前10 min時頸外靜脈輸註生理鹽水5 ml·kg-1·h-1至再灌註120 min;低、中、高劑量瑞芬太尼組(L組、M組、H組)缺血前10 min時頸外靜脈輸註瑞芬太尼1、5、10μg·kg-1·min-1至再灌註120 min,餘處理同IR組.再灌註120 min時處死動物取心髒,採用Western blot法測定心肌細胞覈NF-κB的錶達水平,以反映其活性,觀察心肌組織病理學結果.結果 與S組比較,其餘各組NF-κB活性升高(P＜0.05);與IR組比較,L組、M組和H組NF-κB活性降低(P＜0.05),L組、M組和H組NF-κ:B活性依次降低(P＜0.05);病理學結果顯示:L組、M組和H組心肌缺血再灌註損傷程度較IR組減輕,且隨劑量增加,損傷逐漸減輕.結論 靜脈輸註瑞芬太尼可通過降低NF-κB活性減輕兔心肌缺血再灌註損傷,其效應呈劑量依賴性.
목적 탐토서분태니대토심기결혈재관주시NF-κB활성적영향.방법 건강성년신서란대백토50지,월령2～3월,체중2.0～2.5 kg,수궤분위5조(n=10):가수술조(S조)좌관상동맥전강지지천선불결찰;결혈재관주조(IR조)관상동맥전강지천선결찰30 min,재관주120 min;S조화IR조재결혈전10 min시경외정맥수주생리염수5 ml·kg-1·h-1지재관주120 min;저、중、고제량서분태니조(L조、M조、H조)결혈전10 min시경외정맥수주서분태니1、5、10μg·kg-1·min-1지재관주120 min,여처리동IR조.재관주120 min시처사동물취심장,채용Western blot법측정심기세포핵NF-κB적표체수평,이반영기활성,관찰심기조직병이학결과.결과 여S조비교,기여각조NF-κB활성승고(P＜0.05);여IR조비교,L조、M조화H조NF-κB활성강저(P＜0.05),L조、M조화H조NF-κ:B활성의차강저(P＜0.05);병이학결과현시:L조、M조화H조심기결혈재관주손상정도교IR조감경,차수제량증가,손상축점감경.결론 정맥수주서분태니가통과강저NF-κB활성감경토심기결혈재관주손상,기효응정제량의뢰성.
Objective To investigate the effects of remifentanil on NF-κB activity in a rabbit model of myocardial ischemia/reperfusion (I/R) injury. Methods Fifty New Zealand white rabbits were randomly divided into 5 groups (n = 10 each): sham operation group (group S); group I/R; low dose of remifentanil group (group L); median dose of remifentanil group (group M); high dose of remifentanil group (group H). In group I/R, L,M and H, myocardial I/R was produced by occlusion of left anterior descending artery for 30 min followed by 120 min reperfusion.In group S and I/R,10 min before ischemia,normal saline was infused at 5 ml·l·h-1 via the external jugular vein until the end of 120 min reperfusion. In group L, M and H, remifentanil was infused at 1, 5 and 10ug·kg·min-1 respectively 10 min before ischemia until the end of 120 min reperfusion,and the other procedures were the same as those in group I/R. The myocardial tissues were taken at the end of 120 min reperfusion for determination of NF-κB expression which was used to reflect the activity of NF-κB and microscopic examination. Results The activity of NF-κB was significantly higher in group I/R, L, M and H than in group S. The activity of NF-κB was gradually decreased with the increase in the dose of remifentanil in group L, M and H compared with group I/R. The microscopic examination showed that remifentanil significantly attenuated I/R-induced injury in a dose-dependent manner. Conclusion Infusion of remifentanil reduces myocardial I/R injury through decreasing the activity of NF-κB in a doee-dependent manner.
