目的 :观察电针刺激对缺血再灌注心肌保护中IL 8的作用机制。方法 :48例行冠脉搭桥术病人随机分为针刺组和对照组。于术前、体外循环转流前、停转流 60min和术毕取右心房血测定IL 8、SOD、MDA。转流前、停转流 60min取右心耳心肌组织

电镜观察心肌超微结构变化。结果 :两组IL 8含量持续上升

针刺组停转流 60min、术毕含量显著低于对照组。SOD、MDA于转流前至术毕呈现下降趋势

其中针刺组转流前SOD较对照组显著升高

而MDA显著降低。电镜观察显示停转流 60min针刺组心肌细胞损伤程度明显小于对照组。结论 :针刺能抑制IL 8的释放

减少氧自由基的产生

减轻受氧自由基的攻击程度

从而对缺血再灌注心肌具有保护作用Objective: To observe the action of IL-8 in electroacupuncture (EA)-produced protective effect in patients undergoing coronary artery bypass grafting (CABG).Methods: Forty-eight patients undergoing CABG were randomized into EA group (n=24) and control group (n=24). In EA group

bilateral Neiguan (PC 6)

Lieque (LU 7) and Yunmen (LU 2) were punctured and stimulated electrically with parameters of 3～4 Hz

0.5～1 mA and duration of 20～30 min. Blood samples were taken from the right cardiac atrium before operation

before cardiopulmonary bypass (CPB)

60 min after CPB and at the end of operation in order to detect contents of IL-8

malondialdehyde (MDA) and superoxide dismutase (SOD). Myocardial tissues of the right atrium were taken before and 60 min after CPB in order to observe ultrastructural changes of myocytes. Results:Self-comparison between pre-operation

pre-CPB and post-CPB and post-operation in each group showed that the contents of IL-8 in both groups increased considerably 60 min following CPB and operation (P<0.05). IL-8 levels 60 min after CPB and at the end of operation in EA group were significantly lower than those of control group (P<0.05). The activity of SOD and the content of MDA before CPB in each group increased significantly compared with pre-operation and tended to decrease from 60 min after CPB to the end of operation (P<0.05). Comparison of two groups showed that SOD and MDA levels of EA group before CPB were significantly higher than those of control group (P<0.05). Electronmicroscopic observation showed that the myocardial cellular damage (swelling of mitochondria

myofibril breaking

etc.) was lighter in EA group than that in control group.Conclusion: EA can suppress the release of blood IL-8

which reduces the production of oxygen free radical and relieves its attack on myocytes

preventing the myocardium from ischemia-reperfusion injury.