腺苷A1受体激动剂预处理对兔心肌缺血再灌注损伤的延迟保护作用

【目的】探讨腺苷A1受体激动剂（2-氯环戊腺苷,CCPA）预处理对兔心肌缺血再灌注损伤的延迟保护作用。【方法】30只健康新西兰雄性大白兔随机分成3组：假手术组（C组）、缺血再灌注组（I／R组）、CC—PA组（P组）,每组10只。C组仅行左冠脉套线而不阻断160min,I／R组行左冠脉阻断40min,再灌注120min,P组在静注CCPA 0．1mg／kg 24h后,处理同I／R组。各组分别于左冠前降支阻断前20min（T1）、左冠前降支阻断20min（T2）、左冠前降支阻断40min（T3）、心肌再灌注1h（T4）、心肌再灌注2h（T5）五个时点抽取颈内动脉血测定血清中肌钙蛋白Ⅰ（cTnI）含量。再灌注120min后,测心肌超氧化物歧化酶（SOD）活性、丙二醛（MDA）含量和心梗面积,电镜下观察细胞超微结构变化。【结果】与I／R组比,P组cTnI和MDA降低（P〈0．05）,SOD增高（P〈0．05）,心肌梗死面积减少（P〈0．05）,细胞结构损伤减轻。【结论】CCPA延迟预处理对兔心肌缺血再灌注损伤有保护作用。

Effect of Adenosine A1 Receptor Agonist Delayed Preconditioning on the Protection of Myocardial Ischemia Reperfusion Injury in Rabbits

[Objective] To investigate the effect of adenosine A1 receptor agonist（2-chloro-N6-cyclopentyladenosine,CCPA） delayed preconditioning on the protection of rabbit myocardial injury during ischemia reper fusion. [Methods] Thirty New Zealand male white rabbits were randomly assigned to Sham group, I/R group and CCPA group. Group CCPA was given CCPA 0.1mg/kg before myocardial ischemia. Twenty four hours later, the I/R and CCPA underwent 40rain of coronary occlusion followed by 2h of reperfusion. Blood samples were taken from arterial line at 20min before occlusion（T1 ）, 20min after occlusion（T2 ）, 40min after occlusion （T3）, lh after reperfusion（T4） and 2h after reperfusion（T5 ） for determination of plasma levels of cTnI. At the end of the reperfusion, infarct size（IS） and area at risk（AAR） were defined by Evans and TTC staining. The heart was harvested to observe the ultrastructures under electron microscopy. Plasma superoxide dismutase（SOD） activity and malondialdehyde（MDA） were determined at the end of reperfusion. [Results]The CCPA （ P 〈0.05） reduced infarct size（22.1%±3.8% in group CCPA） of left ventricular area at risk as con〉 pared with the I/R （41.8%±4.3% in group I/R）. The injury of group I/R was worse than that of group CC PA under light microscope. Group CCPA had higher level of SOD and lower level of MDA and cTnI than those of group I/R. [ConclusionlCCPA preconditioning induces late cardioprotection against postischemic reperfusion injury in rabbits.