摘要
目的探讨尤瑞克林后处理是否具有减轻心肌缺血再灌注损伤的作用及其机制。方法建立家兔缺血再灌注模型,随机分为3组,A组为假手术组(n=5),B组为I/R组(n=10),C组为尤瑞克林后处理组(n=10)。分别在缺血前、缺血30 min、再灌注2 h末检测血浆磷酸肌酸激酶(CK)和丙二醛(MDA)活性;实验结束时,测定各组心肌梗死面积并检测心肌组织中髓过氧化物酶(MPO)的活性。结果 C组心肌梗死面积和心肌组织中MPO活性明显低于B组(P均<0.05);再灌注2 h末C组血浆中CK和MDA活性明显低于B组(P均<0.01)。结论缺血再灌注前给予尤瑞克林后处理可以减轻心肌的损伤,减小梗死面积。这种保护作用可能与尤瑞克林抗炎、保护血管内皮功能、减轻Ca2+超载、减轻氧化损伤有关。
Objective It is to explore whether the postconditioning of Levosimendan（LEV） has cardioprotective effects a- gainst ischemia and reperfusion injury and the potential mechanism involved. Methods Ischemia and repcrfusion injury rat models were established and were randomly divided into 3 groups： sham operated group（ n = 5 ） （group A） , I/R group（ n = 10） （group B） , LEV postconditioning group（ n = 10） （group C）. Plasma creative kinase（CK） activity and malondialdehyde （MDA） activity were measured at baseline, the end of isehemia, and after 2 h of reperfusion respectively. In the end of the ex- periment, the myocardial infarct size and tissue myeloperoxidase （MPO） activity were determined. Results Myocardial infarct size and MPO activity in the ischemie area was significantly reduced in C group compared to B group（P 〈0.05）. Plasma CK activity and MDA activity were significantly lower at 2 h of reperfusion in C group than that in B group（P 〈 0.01 ）. Conclu- sion Postconditioning of Levosimendan applied just before the onset of coronary artery reperfusion provides potent myocardial infarct size reduction and cardio-protective effect. The potential mechanism of this phenomenon might be associated with de- creasing the injury by avoiding Ca2＋ ovdrload and decreasing peroxidation.
出处
《现代中西医结合杂志》
CAS
2013年第28期3093-3094,3161,共3页
Modern Journal of Integrated Traditional Chinese and Western Medicine
关键词
尤瑞克林
后处理
缺血再灌注损伤
levosimendan
postconditioning
ischemia/reperfusion injury
