Gross Eric R, Gross Garrett J
Medical College of Wisconsin, Department of Pharmacology and Toxicology, 8701 Watertown Plank Road, Milwaukee, WI 53226, United States.
Cardiovasc Res. 2006 May 1;70(2):212-21. doi: 10.1016/j.cardiores.2005.12.019. Epub 2006 Jan 31.
The cardioprotection afforded by ischemic preconditioning (IPC) and ischemic postconditioning (PC) are receptor mediated. In this review, we will focus on the major ligand classes and receptors that contribute to IPC and PC-induced cardioprotection. Ligand classes discussed include adenosine, bradykinin, opioids, erythropoietin, adrenergics and muscarinics. The cardioprotective therapeutic window of each ligand class will also be summarized, with particular focus as to whether ligands are protective when administered at or close to the time of reperfusion. Information will primarily be directed at studies in which infarct size reduction is the gold standard to assess the efficacy of IPC and PC. Myocardial stunning is a less robust endpoint for assessing cardioprotection and the use of this endpoint is only limited to studies with human tissue where infarct size assessment is not possible. Receptor cross-talk between ligands and the common signaling pathways involved for these ligands will also be briefly discussed.
缺血预处理（IPC）和缺血后处理（PC）所提供的心脏保护作用是由受体介导的。在本综述中，我们将重点关注促成IPC和PC诱导的心脏保护作用的主要配体类别和受体。所讨论的配体类别包括腺苷、缓激肽、阿片类物质、促红细胞生成素、肾上腺素能物质和毒蕈碱类物质。还将总结每种配体类别的心脏保护治疗窗，特别关注配体在再灌注时或接近再灌注时给药是否具有保护作用。信息将主要针对以梗死面积缩小作为评估IPC和PC疗效的金标准的研究。心肌顿抑是评估心脏保护作用的一个不太可靠的终点，该终点的使用仅限于无法进行梗死面积评估的人体组织研究。还将简要讨论配体之间的受体相互作用以及这些配体所涉及的共同信号通路。
