摘要
目的 探讨缓激肽 (BK)的心肌延迟性保护作用及其与延迟相缺血预适应的关系 .方法 2 8只健康新西兰兔 ,随机分为 4组 . 组 (对照组 ) :建立动物模型后关胸 ,2 4h后心肌缺血 40 min,再灌注 6 0 min. 组 (缺血预适应组 ) :建立动物模型后心肌缺血 5 m in,再灌注 10 min,共重复 4次 ,余同 组 . 组 (缓激肽组 ) :建立模型后给予 BK左室内灌注 5 0 μg· kg- 1 · min- 1 ,共 10 min,其余同 组 . 组 (Hoe140组 ) :第 1日建立模型后给予 Hoe140 10 μg· kg- 1 静注 ,其余同 组 .结果 缺血预适应组及缓激肽组心肌梗死面积与心肌危险区面积之比 (% )分别为 14.1± 2 .3,2 1.2± 2 .2 ,较对照组(33.6± 3.1)明显下降 (P<0 .0 5 ) ,Hoe140组完全抑制了缺血预适应的延迟相心肌保护作用 .结论 BK对心肌具有延迟相保护作用 ,内源性 BK参与了延迟相缺血预适应心肌保护作用 .
AIM To investigate the delayed cardioprotective action and the role of bradykinin (BK) in delayed ischemic preconditioning. METHODS 28 New Zealand white rabbits were randomly divided into four groups. In Group Ⅰ were sham operated animals, who received vehicle only. In Group Ⅱwere the preconditioning animals, who received four times of 5 min occlusion and 10 min reperfusion. In Group Ⅲ, the animals were sham operated and received bradykinin. In Group Ⅳ, the animals were preconditioned and received Hoe140. RESULTS Infarction risk zone ratios (%) of the preconditioned group and the BK group were 14.1±2.3 and 21.2±2.2 respectively, reducing significantly compared with that of the control group (33.6±3.1). The protective action of preconditioning was inhibited by Hoe140. CONCLUSION Bradykinin can induce delayed cardioprotection and endogenous bradykinin participates in the delayed ischemic preconditioning.
出处
《第四军医大学学报》
2000年第3期317-319,共3页
Journal of the Fourth Military Medical University
