高胸段硬膜外阻滞对猪急性心肌缺血/再灌注损伤的保护作用

The protective effect of high thoracic epidural anesthesia on myocardium agamst acute ischemia-reperfusion injury in pigs

目的 探讨高胸段硬膜外阻滞(HTEA)对心肌缺血/再灌注损伤的保护作用。方法 20只家猪随机分为两组,结扎左冠状动脉前降支(LAD)造成缺血40 min后再灌注6 h,实验组(n=10)结扎前硬膜外腔注入0.5％布比卡因2 ml;对照组(n=10)结扎前硬膜外腔注入生理盐水2 ml。测定心率(HR)、平均动脉压(MAP)、中心静脉压(CVP)、血浆超氧化物歧化酶(SOD)活性、血清丙二醛(MDA)浓度、心肌乳酸(LA)释放量。结果 (1)实验组硬膜外阻滞的HR减慢22％,MAP、CVP分别降低25％和28％,而对照组血液动力学无明显变化。(2)实验组SOD活性变化不显著,再灌注5 h、6 h活性升高(P<0.01);MDA浓度在4 h降至最低点(P<0.05);对照组SOD活性明显降低(P<0.05),MDA含量明显增加(P<0.05)。(3)两组心肌LA释放量在开放前达到高峰,之后随着供血、供氧的恢复逐渐下降,但实验组明显低于对照组(P<0.01)。(4)开始再灌注时由于发生室颤实验组死亡1只,对照组死亡4只(P<0.05)。结论HTEA可以减轻心肌缺血,再灌注损伤,其机制与保护SOD活性、降低心肌氧耗及脂质过氧化程度有关。

Objective To evaluate the protective effect of high thoracic epidural anesthesia (HTEA) on myocardium against acute ischemia-reperfusion injury.Methods Twenty healthy male pigs, aged 2-3 months, weighing 20-25 kg were randomly divided into two groups:HTEA group ( I , n = 10) and control group ( II , n = 10) .The animals were premedicated with intramuscular ketamine 20 mg · kg-1 . Anesthesia was induced with thiopentone 10 mg · kg-1 and maintained with 1% procaine + 0.1% succinylcholine infusion after tracheal intubation. Epidural puncture was performed at T3.4 .A catheter was inserted into epidural space for 5 cm in a cephalad direction. The position of the catheter in epidural space was confirmed by X-ray with contrast medium. HTEA group received 0.5% bupivacaine 2 ml epidurally space before occlusion of coronary artery, while in control group normal saline 2 ml was injected instead of 0.5% bupivacaine. Myocardial ischemia-reperfusion model was prepared according to Davis's method. Left anterior descending branch (LAD) of coronary artery was clamped for 40 min then released for reperfusion. Myocardial ischemia was confirmed by S-T segment elevation > 0.5 mV and change in color of myocardium. Blood samples were taken from right atrium for determination of plasma SOD activity and plasma MDA level and from coronary sinus and artery for determination of blood lactate level before occlusion of LAD ( T0 ) , before reperfusion (T1),1,2,3,4,5,6 h after reperfusion (T2-7 ) . Myocardial lactate production was calculated from the difference between coronary sinus and arterial blood lactate concentrations. Results ( 1) In HTEA group HR, MAP and CVP decreased by 22% , 25% and 28% after epidural blockade, while in control group there was no significant change after epidural saline. (2) In HTEA group plasma SOD activity started increasing at T6 and blood MDA level decreased at T4 and T5, whereas in control group blood SOD activity started decreasing and blood MDA level started increasing at T3 . (3) Myocardium released no lactate before ischemia. Myocardial lactate release greatly increased during ischemia and started decreasing after reperfusion in both groups. But myocardial lactate production was significantly less in HTEA group than that in control group. (4) One animal died from ventricular fibrillation at the beginning of reperfusion in HTEA group while in control group four animals died. Conclusion HTEA can alleviate the myocardial ischemia-reperfusion injyry by blocking sympathetic nervous activity.