| Objective: To evaluate the effect of HTEA on the protection of myocardial ischemia/referfusion injury, we observed the hemodynamic change, the activity of SOD, the concentration of MDA and the release of LA. Methods: 20 swine aged from 2 to 3 months and weighed from 20Kg-25Kg were divided randomly into two groups. Animals in the experimental group (n=10) received 2 ml of epidural 0.5% Bupivacain; Animals in the control group (n=10) received 2ml of epidural normal saline. Referring to the experiment model made by Davis: each of the swine was premedicated intramuscularly with Ketamine 20mg/Kg before fixing them to the operating table. Animals were anesthetized intravenously with Thiopental 10mg/Kg before trachealing intubation. After the T3-4 puncture of the epidural space with the loss-of-resistance technique an 18-gauge catheter was advanced epidurally 5cm. Correct position of the catheter was verified by radioscopy. The spread of the local anesthetic was determined immediately after insertion of the epidural catheter and verification of its correct position by injecting Isovist300 1ml and Bupivacain 2ml. The range was T1-6. Anesthesia was maintained with 1% Procain and 0.1% Scoline. PETCO2, Standard ECG leadⅡ, HR and MAP were monitored. Separate the right femoral and insert the catheter to measure blood pressure directly. The heart was exposed through cleavage of the breastbone. The right atria was cannulated to monitor CVP and liquid infusion. Meanwhile, the coronary sinus was cannulated from heart main vein for blood sampling. The left anterior descending coronary artery (LDA) was dissected. 2ml of 0.5% epidural Bupivacain was injected in the experimental group; 2ml of epidural normal saline was injected in the control group. The skin temperature was measured 15 min before injection and after injection. After 15 minutes, the LAD was ligated and 40 minutes later it was set free. During the operation, Bupivacain and Normal Saline were injected every 2 hours and CVP was kept at 12cmH2O. The room temperature was controlled at 25℃. Blood samples were taken before ligation, setting free and 1h, 2h, 3h, 4h, 5h, 6h after setting free from right atria to determine the plasma SOD activity and serum MDA concentration. Besides, blood samples were also taken from the coronary sinus and the femoral to determine the release of myocardial LA. The myocardium of the same region was taken for the electron microscope before the occlusion and 6h after setting free. The complete layer was taken to observe the ultrastructure before theocclusion, 40min after the occlusion and 5h after setting free.Results: (1) The age and weight have no prominent difference. (2) HR, MAP and CVP in the experimental group decreased by 22%, 25% and 28% respectively while there was no much change in the control group after blocking.. (3) The activity of SOD didn't change promptly in the experimental group but it began to increase after 5 hours (p<0.01), while in the control group it didn't change promptly before 2h, decreased significantly from 3h-6h (p<0.05-0.01); the concentration of MDA in the experimental group didn't change promptly till 3h, decreased to the minimum at 4h(p<0.05), then it was not prominent from 5h to 6h; while in the control group the concentration of MDA sharply increased; compared with control group, the activity of SOD increased sharply from 2h to 6h and the concentration of MDA decreased(p<0.01). (4) The myocardial cell took LA from blood so the release was negative; the release of LA in both of the two groups reached peak before reperfusion, and then began to decrease with the supply of blood and oxygen. But there was obvious difference (p<0.01) between the 2 groups. (5) One swine died in the experimental group when the coronary artery was set free because of ventricular fibrillation, while in the control group four swine got dead (p<0.05). (6) Myocardial ultrastructure: before occlusion, in the experimental group the myocardial fiber and arrayed in order and edema, but the |
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