| Objective:To evaluate the protection of thoracic epidural anesthesia during myocardial ischemia reperfusion injury caused by open heart surgery, we observed the hemodynamic change, spontaneously rebeating of the heart, the level of cTnI, the level of CK-MB, the concentration of MDA, the activity of SOD and the change of myocardial ultrastructure. Learning on the clinic experiments, our study try to interpret the myocardial protecting mechanisms of thoracic epidural anesthesia during myocardial ischemia reperfusion injury caused by open-heart surgery. To find a better method to protect the myocardium during open-heart surgery with cardiopulmonary bypass.Methods:Twenty patients scheduled for repair of ventricular septal defect (VSD) and atrial septal defect (ASD) were randomly divided into two groups: the control group (group I；n=10) and the experiment group (group II; n=10). The patients of the control group were used general anesthesia while the patients of the experiment group were used thoracic epidural anesthesia combined with general anesthesia. A catheter was inserted into thoracic epidural space at T3-4 or T4-5 in patients of the experiment group in the morning of surgery. When the thoracic epidural anesthesia was confirmed to be effective after injecting 1% lidocaine 3ml, general anesthesia was induced with intravenous Midazolam 0.15mg?kg -1, fentanyl 5μg?kg -1 and vecuronium 0.1mg?kg -1. Then anesthesia maintained with intravenous administration of vecuronium,fentanyl ( add up to 30μg?kg -1) and inhalation of isoflurane 1.0-1.5MAC. At the same time, 0.2% ropivacaine 5ml was injected into the thoracic epidural space every 1h. The time must exceed 1h from the end of the catheter was inserted into thoracic epidural space to heparinization. All procedures in the control group were similar to those of the experiment group except for thoracic epidural anesthesia. Standard ECG leadⅡ, HR,MAP,CVP, SpO2, PETCO2 and the temperature of patient were continuously monitored. Before using medicine in the operating room, we measured the HR, MAP and CVP as baseline. The time of clamping aorta, cardiopulmonary bypass and operating, the spontaneously rebeating of heart and the situation of electrocution defibrillation were recorded.Blood samples were taken from artery after induction (T0), before cardiopulmonary bypass (T1), 5min after opening aorta (T2), 30min after opening aorta (T3), 6h after termination of cardiopulmonary bypass (T4), 24h after termination of cardiopulmonary bypass (T5) and 48h after termination of cardiopulmonary bypass (T6) for determination of the level of cTnI, the level of CK-MB, the concentration of MDA and the activity of SOD. The myocardium of right atrial was taken to observe the ultrastructure before cardiopulmonary bypass (T1) and 30 min after opening aorta (T3). Results1 the effect of clinic1.1 The age and weight of the two groups have no significant difference (P>0.05).1.2 The change of hemodynamic: HR,MAP,CVP were kept unsignificantly changed in the control group while those were decreased by 20%, 23% and 25% respectively in the experiment group compared with those before thoracic epidural administration ( baseline ).1.3 Rate of the heart spontaneously rebeating in the control group was 60% (four patients occurred ventricular fibrillation and need electrocution defibrillation) while those in the experiment group was 100%.There was significant difference between the control group and the experiment group (P<0.05).2 The biochemistry of myocardium2.1 The change of cTnI level: There was no significant difference between T0 in the two groups (P>0.05). Compared with T0, cTnI level gradually increased, there was significant and extraordinarily significant difference at T1 and T2~T6 in the control group; cTnI level in the experiment group gradually increased beginning of T2 and there was extraordinarily significant difference at T2~T6. CTnI level at T2~T6 was notably lower in the experiment group than that in the control group (P<0.01)...
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