Cardioprotection with adenosine A2 receptor activation at reperfusion.
Cardioprotection with adenosine A2 receptor activation at reperfusion.
复制标题
再灌注时腺苷 A2 受体激活的心脏保护作用。
DOI：
10.1097/01.fjc.0000188161.57018.29
复制
发表时间：
2005
影响因子：
3
通讯作者：
Downey,JamesM
中科院分区：
文献类型：
--
作者：
Xu,Zhelong;Mueller,RobertA;Park,Sung-Sik;Boysen,PhilipG;Cohen,MichaelV;Downey,JamesM
在急性心肌梗塞的临床环境中，很少可能进行预缺血治疗。因此，为了成功地挽救心肌免于梗塞，要求在缺血开始后或再灌注开始时应用保护性干预措施必须有效。不幸的是，尽管大量实验数据表明各种干预措施在再灌注时具有心脏保护作用，但尚未建立临床适用的具体疗法。然而，几个实验室的最新数据表明，再灌注时给予腺苷及其类似物可以显着保护心脏免受缺血/再灌注损伤。虽然实验数据表明，腺苷 A 2 受体激活、抗中性粒细胞作用、自由基产生减弱、一氧化氮 (NO) 可用性增加、PI3 激酶/Akt 通路和 ERK 激活、预防线粒体损伤和抗凋亡作用等因素可能与腺苷或其类似物的保护作用有关，但确切的受体亚型、详细的信号传导机制以及这些单独因素之间的相互作用仍然未知。对这些未解决问题的明确答案将为再灌注时心脏保护机制提供深入的见解，并且对于制定成功的治疗策略来挽救急性心肌梗死患者的缺血心肌至关重要。
Pre-ischemic treatment is seldom possible in the clinical setting of acute myocardial infarction. Thus, to successfully save myocardium from infarction, it is required that protective interventions must be effective when applied after ischemia has begun or at the onset of reperfusion. Unfortunately, in spite of a large body of experimental data showing that various interventions are cardioprotective at reperfusion, no specific therapy has yet been established to be clinically applicable. However, recent data from several laboratories have shown that adenosine and its analogues given at reperfusion can markedly protect the heart from ischemia/reperfusion injury. While the experimental data suggest that factors such as adenosine A 2 receptor activation, anti-neutrophil effect, attenuation of free radical generation, increased nitric oxide (NO) availability, activation of the PI3-kinase/Akt pathway and ERK, prevention of mitochondrial damage, and anti-apoptotic effects may be involved in the protective effect of adenosine or its analogues, the exact receptor subtype (s), the detailed signaling mechanisms, and interaction between those individual factors are still unknown. A definite answer to these unsolved problems will offer insights into the mechanisms of cardioprotection at reperfusion, and will be critical for developing a successful therapeutic strategy to salvage ischemic myocardium in patients with acute myocardial infarction.