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目的 :研究缓激肽 (BK)是否参与了大鼠心肌缺血预处理 (IP)。方法 :观察缺血再灌注组、缺血预处理组、缺血再灌注前给予缓激肽组、缺血再灌注前给予缓激肽及缓激肽B2 受体拮抗剂B1650 组以及缺血预处理时加B1650 组各组缺血复灌前后心功能变化 ,并且检测复灌末丙二醛 (MDA)和超氧化物歧化酶 (SOD)的变化。结果 :缺血再灌注前给予缓激肽可明显减轻再灌注损伤 ,使心脏收缩及舒张功能明显高于缺血再灌注组 ,MDA生成下降 ,SOD活性增加 ;加B1650 ,这种保护作用消失。结论 :缓激肽参与缺血预处理心肌保护的作用是通过激活缓激肽B2 受体介导的
AIM: To investigate whether bradykinin (BK) is involved in myocardial ischemic preconditioning (IP) in rats. Methods: The ischemia / reperfusion group, the ischemic preconditioning group, the bradykinin group before ischemia reperfusion, the bradykinin and bradykinin B2 receptor antagonist group B1650 before ischemia reperfusion, The changes of cardiac function before and after ischemia reperfusion in B1650 group were also measured. The changes of malondialdehyde (MDA) and superoxide dismutase (SOD) at the end of reperfusion were measured. Results: Pretreatment with bradykinin could significantly reduce the reperfusion injury, and the cardiac systolic and diastolic function was significantly higher than that of the ischemia-reperfusion group. The generation of MDA was decreased and the activity of SOD was increased. When B1650 was added, the protective effect disappeared. CONCLUSION: The effect of bradykinin on ischemic preconditioning myocardial protection is mediated through the activation of bradykinin B2 receptor