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作 者:徐延敏[1] 黄体钢[1] 陈元禄[1] 李广平[1]
出 处:《天津医药》2003年第10期663-665,共3页Tianjin Medical Journal
摘 要:目的 :探讨卡托普利对Langendorff灌注大鼠全心缺血—再灌注损伤的保护作用及机制。方法 :采用Langendorff离体全心灌流装置 ,模拟缺血 -再灌注 ,观察卡托普利对大鼠全心缺血 -再灌注引起的心律失常的作用及体内CPK、LDH、MDA、SOD及AngII含量的变化。结果 :卡托普利减少缺血及再灌注期心律失常的发生,加快再灌注期高度房室传导阻滞的恢复。缺血期:CPK及LDH缺血 -再灌注(B组)组较对照组(A组)明显增加,卡托普利治疗组(C组)较B组显著降低,再灌注期:CPK及LDHB组较A组明显增加 ,C组较B组明显降低,心肌组织MDA ,AngII的含量B组明显高于A组 ,C组明显低于B组 ,而SOD含量两组比较无显著性差异。结论:卡托普利具有拮抗离体大鼠全心缺血 -再灌注损伤的作用 ,拮抗作用是通过抑制血管紧张素转换酶(ACE)而抑制AngII的生成 。Objective:To investigate the cardioprotective and mechanisms of Captopril on Langendorff per-fused in whole isolated rat hearts.Methods:Langendorff perfused system was used to investigate the effect of Captopril on CPK,LDH,MDA,SOD,and Ang II in whole isolated rat hearts and occurrence of arrhythmi-a.Results:Captopril decreased incidence of arrhythmia in ischemic and reperfusion periods,and improved atrial ventricular block recovery in reperfusion period.During ischemic period,CPK and LDH in group B increased significantly compared with that in group A,but greatly decreased in group C compared with that in group B.During reperfusion period,CPK and LDH increased significantly in group B compared with that in group A,however decreased in group C compared with that in group B.The contents of MDA and Ang II of myocardial tissue in group B were higher than that in group A.The content of MDA of myocardial tissue in group C was much lower than that in group A.The content of MDA of myocardial tissue in group C was much lower than that in group A.SOD had no significant change in two groups.Conclusion:Captopril against is-chemic_reperfusion injury in whole isolated rat hearts,those beneficial effects are mediate primarily by the in-hibition of Angiotensin II formation and inhibited oxygen free radical scavenging potential.
关 键 词:心肌缺血 再灌注损伤 卡托普利 Langendorff灌注 血管紧张素Ⅱ
分 类 号:R542.2[医药卫生—心血管疾病] R972[医药卫生—内科学]
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