论文部分内容阅读
目的 :明确正常人及AMI溶栓前后与SOD、LPO含量的关系。早期溶栓可使 6 0 %～ 70 %的梗塞相关动脉再通 ,但溶栓再通后的心肌再灌注损伤却降低了溶栓成功的净效应 ,甚至导致梗塞范围扩大 ,其机制与氧自由基 (OFR)代谢紊乱有关。方法 :本研究通过测定 15例心肌梗塞病人溶栓前后静脉血超氧化物歧化酶 (SOD)活力和脂质过氧化物 (LPO)的含量 ,以观察心肌梗塞溶栓前后心肌再灌注损伤与氧自由基的关系 ,并设正常对照组。结果 :溶栓治疗前LPO、SOD均明显高于对照组 ,溶栓治疗后 2、6小时SOD活性明显低于溶栓前 ,LPO于治疗后浓度较溶栓前显著升高 ,尤以 12小时升高显著。结论 :急性心肌梗塞(AMI)溶栓治疗致心肌再灌注损伤与氧自由基之间有密切关系。本文通过测定 15例AMI溶栓前后静脉血脂质过氧化物(LPO)、超氧化物歧化酶 (SOD)的动态变化 ,明确溶栓前后与SOD及LPO含量之间的关系
Objective: To clarify the relationship between SOD and LPO content before and after thrombolysis in normal subjects and AMI. Early thrombolysis can cause 60% to 70% of infarct-related arteries recanalization, but myocardial reperfusion injury after thrombolytic recanalization has reduced the net effect of successful thrombolysis and even led to the expansion of infarct size, the mechanism of which is oxygen free (OFR) metabolism disorders related. Methods: Fifteen patients with myocardial infarction before and after thrombolysis were measured venous blood superoxide dismutase (SOD) activity and lipid peroxide (LPO) levels in myocardial infarction before and after thrombolysis to observe myocardial reperfusion injury with oxygen Free radicals, and set the normal control group. Results: The levels of LPO and SOD before thrombolytic therapy were significantly higher than those of the control group. The activity of SOD was significantly lower at 2,6 hours after thrombolytic therapy than before thrombolytic therapy. LPO after treatment was significantly higher than that before thrombolysis, especially at 12 hours Significantly increased. Conclusion: There is a close relationship between myocardial ischemia reperfusion injury and oxygen free radical in acute myocardial infarction (AMI) thrombolytic therapy. In this paper, we measured the changes of venous blood lipid peroxidation (LPO) and superoxide dismutase (SOD) in 15 AMI patients before and after thrombolysis, and clarified the relationship between SOD and LPO content before and after thrombolysis