异丙酚加小剂量芬太尼对体外循环手术心肌核因子-κB的影响

目的 :观察异丙酚加小剂量芬太尼对小儿体外循环心脏手术心肌核因子 κB(NF κB)和细胞间粘附分子1(ICAM 1)的影响 ,探讨其减轻心肌缺血再灌注损伤的可能机制。方法 :2 0例体外循环 (CPB)下手术治疗的先天性心脏病 (ASD、VSD)病人 ,随机等分为异丙酚加小剂量芬太尼联合组 (PF组 ,异丙酚 2mg·kg- 1 ·h- 1 加芬太尼 2 0～ 30μg·kg- 1 )和大剂量芬太尼组 (HF组 ,芬太尼 6 0～ 70 μg·kg- 1 )。检测上、下腔静脉置管时和开放主动脉 30min时右心耳心肌NF κB和ICAM 1的表达 ,在切皮前 (T0 )、CPB前 (T1 )、主动脉阻断 2 5min(T2 )、主动脉开放 30min(T3)、CPB后12 0min(T4 )和术后 2 4h(T5)的血清过氧化物歧化酶 (SOD)活性 ,并记录术后气管拔管时间及恢复情况。结果 :在主动脉开放 30min时 ,两组心肌NF κB和ICAM 1的灰度值比CPB前显著降低 (P <0 .0 5 ) ,但PF组心肌NF κB及ICAM 1的灰度值显著高于HF组 (P <0 .0 5 )。在T2 、T3和T4 时 ,PF组SOD活性值显著高于HF组 (P <0 .0 5 )。术后两组病人均顺利康复 ,但PF组病人术后气管导管拔出时间较HF组早 (P <0 .0 5 )。结论 :异丙酚加小剂量芬太尼复合麻醉可能通过抑制心肌NF κB、ICAM 1的表达与活性 ,对缺血再灌注心肌产生保护作用

Effect of Propofol Plus Low Dose of Fentanyl Anesthesia on NF-κB Activation in Myocardium with Cardiopulmonary bypass Heart Surgery

Objective: To investigate the effect of propofol plus low dose of fentanyl anesthesia on nuclear factor κappa B (NF κB)and intercellular adhesion molecule 1(ICAM 1) in myocardium in children with cardiopulmonary bypass (CPB) heart surgery and furthermore to explore its possible mechanisms of reducing myocardium ischemic reperfusion injury. Methods: 20 children with congenital heart disease(ASD,VSD) and elective CPB heart surgery were examined and divided randomly into either low dose of fentanyl plus propofol anesthesia group(n=10) or high dose of fentanyl anesthesia group(n=10). At the time of intubatton pre CPB and reperfusion 30 min,the myocardial samples were taken to investigate and compare variation of NF κB,ICAM 1, and the serum superoxide dismutase(SOD) activity were investigated at six different points. Results: Myocardial activation of NF κB,ICAM 1 in PF group were obviously lower than that in HF group. The activity of SOD in HF group was significantly lower than that in PF group at the time point of T 2,T 3,T 4. Extubation was earlier in PF group than that in HF group. Conclusion: This study showes that propofol plus low dose of fentanyl anesthesia could protect the ischemia myocardium through inhibiting the activity of myocardium NF κB and ICAM 1.