| Objective: Myocardial protection has been the hot research of open heart surgery under cardiopulmonary bypass(CPB). Postoperative cardiac function obstacle is connect with primary disease, myocardial ischemia during CPB and ischemia-reperfusion injury, surgical trauma and other factors. Ischemia-reperfusion injury is an important factor. Studies have reported Recombinant human erythropoietin(r Hu EPO) pretreatment has protective effect in myocardial ischemia-reperfusion injury, but research of r Hu EPO pretreatment myocardial protection in open-heart surgery is less. Therefore, this topic through the observation of influence on cardiac troponin I(c Tn I), creatine kinase MB(CK-MB) and the myocardial cell ultrastructure change by r Hu EPO pretreatment during perioperation of rheumatic heart valve disease to explore the myocardial protection effect of r Hu EPO pretreatment.Methods: Into the group of patients with rheumatic heart valve(double valve replacements) 40 cases, aged 40~60 years old, preoperative cardiac function level II or III(NYHA). No kidney dysfunction, thyroid disease, diabetes and other metabolic disorder; No angina pectoris, myocardial infarction, hypertension, etc.; No long-term use of glucocorticoid and serious infectious disease. Divided into a control group(group A) and three experimental group(group B,C,D) using random numbers table, 10 cases in each group. All patients were operated in intravenous inhalational anesthesia moderate hypothermic and moderate blood dilution. Experimental group began r Hu EPO subcutaneous injection once a day from 3 days before operation. Group B is 50u/Kg each time, group C is 100u/Kg, group D is 200u/Kg. In the control group(group A) no special treatment. Take the venous blood samples at before anesthesia induction(T0), aortic open(T1), 2h after aorta open(T2), 6h after aortic open(T3), 12 h after aortic open(T4), 24 h after aortic open(T5), 36 h after aortic open(T6), 72 h after opening the aorta(T7), 96 h after opening the aorta(T8) and 120 h after opening the aorta(T9). Detection blood routine, c Tn I, CK-MB. In three time points(blocking aorta, 30 min after aortic and 60 min after aortic) took three small pieces from right atrium comb muscle tissue respectively to check the myocardial cell ultrastructure change.Results: All patients with no complication and were recovered. Difference in general data of the four groups had no statistical significance(P>0.05). All patients serum c Tn I and CK-MB were normal range before anesthesia induction, begin to rise at T0, increased significantly at T2, reach the peak at T4, then gradually decline, and close to normal at 120 h and 72 h after opening respectively. Intra-group c Tn I and CK-MB concentration at T1、T2、T3、T4、T5、T6、T7、T8 and T9 significantly higher than the T0(P<0.05). At the same time points, compare between the test group and control group: at T1、T2、T3、T4、T5、T6、T7、T8 and T9, c Tn I and CK-MB concentration significantly lower than the control group(P<0.05). And the higher r Hu EPO, the lower c Tn I and CK-MB concentration(P<0.05). As the blocking time extend, the muscle wire, sarcomere, mitochondria and sarcoplasmic reticulum damage increased gradually. And the higher r Hu EPO, the lower damage.Conclusion:1. Serum c Tn I, CK-MB were normal before anesthesia induction. It is begins to rise when the aorta block, significantly increase at 2h after opening to the aorta and reach the peak at 12 h after opening, then gradually decline, and close to normal at 120 h and 72 h after opening respectively.2. RHu EPO pretreatment can reduce serum c Tn I and CK-MB of the patient suffered CPB. It also can reduce myocardial ischemia and hypoxia and ischemia-reperfusion injury, and has myocardial protection with dose dependent.3. As the blocking time extend, the myocardial cell ultrastructure damage increased gradually. RHu EPO pretreatment can reduce the damage with dose dependent. |
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