缺血后处理、ATP后处理减轻兔缺血再灌注损伤:与腺苷受体激活有关  被引量:6

Cardio-protection of ATP-postconditioning and Postconditioning in Rabbits: Associated with the Activation of Adenosine Receptors

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作  者:刘方[1] 廉哲勋[1] 王永彬[2] 葛毅萍[3] 

机构地区:[1]青岛大学医学院附属医院心内科,青岛266003 [2]青岛大学医学院附属医院急诊科,青岛266003 [3]青岛大学医学院,青岛266003

出  处:《现代生物医学进展》2007年第3期353-355,共3页Progress in Modern Biomedicine

摘  要:目的:近期实验研究显示,在再灌注的早期给予短暂、重复的缺血再灌(缺血后处理Postconditioning)能够减轻心肌再灌注损伤。本实验旨在探明三磷酸腺苷(ATP)用于缺血后处理是否产生上述保护效应,以及了解腺苷受体在此保护作用机制中的地位。方法:家兔开胸后左前降支均给予40min结扎和180min的再灌注,并随机分为5组:(1)对照组;(2)缺血后处理组;(3)ATP后处理组;(4)缺血后处理+SPT(硫苯茶碱)组;(5)SPT对照组。于实验终点测定心肌梗死面积(TTC染色),血浆CK-MB、SOD、MDA含量。结果:和时照组相比,缺血后处理组与ATP后处理组心梗面积减少(p<0.05),CK-MB也显著降低(p<O.05)。在SPT+后处理组,SPT消除了缺血后处理的上述减少心梗面积作用(p<0.05)。此外,在两个后处理组MDA含量明显降低(p<0.05),SOD含量明显升高(p<0.05),同样地,在SPT+后处理组发现SPT取消了缺血后处理的减轻再灌注损伤作用。结论:ATP后处理具有与机械后处理相同的减轻心肌缺血再灌注损伤作用,而SPT消除缺血后处理保护作用的现象提示,该保护作用的机制可能与腺苷受体的激活有关。Objective: Recent experimental studies indicate that application of short, repetitive ischemia only during the onset of reperfusion, i.e, postconditioning (Post-con), attenuates myocardial reperfusion injury. This study was designed to examine whether Adenosine Triphosphate (ATP) has the same cardio-protective effects or not when administered at the onset of reperfusion, and investigate the role of adenosine receptors in the protection by Post-con. Methods: Thirty anesthetized open-chest rabbits were subjected to 40 rain ischemia of the left anterior descending artery (LAD) and 180 rain reperfusion, and assigned to the following five groups: (1)Control; (2)Post-con; (3)ATP-Post; (4) Post + SPT; (5)CON+SPT, Infarct size (TTC staining), the plasma CK-MB, superoxide dismutase (SOD), and lipid peroxidation product malondialdehyde (MDA) were measured at the end of ischemia, Results: Compared with Control, myocardial infarct size was limited (p〈0,05), which was consistent with CK-MB (p〈0,05); SPT alone had no effect on infarct size(CON+SPT vs CON, p〉0.05), However, Post+SPT abrogated the myocardial infarct size reduction in Post-con (p〈0.05). Besides, MDA was lower and SOD higher in Post-con and ATP-Post than those in CON (p〈0.05), respectively, Similarly, Post+SPT abolished these protective effects in Post-con. Conclusions: Our results suggest that ATP can protect the heart from myocardial ischemia/reperfusion injury when administered at the onset of reperfusion and is as effective as mechanical postconditioning. The ability of SPT to block the cardio-protective effects indicates the mechanism of postconditioning's protection may be associated with the activation of adenosine receptors.

关 键 词:缺血再灌注损伤 缺血后处理 腺苷受体 

分 类 号:R5[医药卫生—内科学]

 

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