【摘要】 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 受体介导的更多还原

【Abstract】 Objective The aim of the present study was to determine whether bradykinin has a protective effect during ischemia?reperfusion and involves in ischemic preconditioning in the rat heart.Methods Acute reversible left main coronary artery occlusion was used.Forty healthy SD rats were randomly divided into five groups:(1)ischemia?reperfusion(IR); (2)ischemic preconditioning (IP); (3)treatment with bradykinin before ischemia( BK+IR); (4) bradykinin treatment combined with pretreatment with bradykinin B 2 receptor antagonist B 1650 before ischemia (BK+BKA+IR); (5)ischemic preconditioning combined with B 2 receptor antagonist B 1650 (BKA+IP). Heart function before and after ischemia?reperfusion were examined.We also measured the content of malondialdehyde(MDA) and superoxide dismutase(SOD) at the end of reperfusion.Results Bradykinin reduced the injury induced by ischemia?reperfusion,improved the heart function,decreased the MDA production,increased the SOD activity.Pretreatment with bradykinin B 2 receptor antagonist B 1650 completely abolished the effect of bradykinin or ischemic preconditioning.Conclusion Bradykinin, through B 2 receptors,can protect ischemic myocardium from ischemic injury , and is involved in ischemic preconditioning in our model.更多还原