Protection of myocardial ischemic preconditioning Advances mechanisms.docVIP

Protection of myocardial ischemic preconditioning Advances mechanisms Of: YANG Shu-yan Zhang Zhong Zheng Zhonghua Zhong Xiuhong Li Zhao Micro Keywords: Myocardial; ischemic preconditioning; protection Myocardium subjected to one or several repeated transient ischemic reperfusion, an expression for a long time and then came the enhanced resistance to ischemic injury, called ischemic preconditioning (IPC). Mainly to reduce myocardial infarct size and improve myocardial contractility, and myocardial protection of coronary endothelial cell ultrastructure and reduce the incidence of arrhythmia, the heart faster recovery from reperfusion myocardial stunning and so on. Produced in the early protection after ischemic preconditioning 3 h, the delayed protection in the pre-generated 24 ~ 72 h after ischemia between. IPC mechanism of myocardial protection has not been completely clarified, the data can be divided into specific and non-specific receptor-dependent protection mechanism. This protective mechanism of IPC on the current research status are summarized below. A specific receptor-dependent protection 1.1 adenosine receptor Adenosine receptor A1, A2, A3 three. Where A1, A3 and IPC close, but both mediated by different protection mechanisms and pathways. A1 receptors via activation of phosphoinositide 3-kinase (phosphoinositide 3 kinase, PI3 K) A Kt Bcl 2 pathway mediated by IPC, while the A3 receptor is activated by cAMP-reactive protein (CREB) Bcl 2 and A Kt Bcl 2 pathway mediates IPC 1. Excited by adenosine or adenosine adenosine receptor agonist, increased myocardial tolerance against ischemic injury. Block adenosine A1, A3 receptors, almost completely eliminate the protective effect of ICP 2. IPC by adenosine receptors and protein kinase C (PKC) and inducible nitric oxide synthase (iNOS) in the activation. 1.2 bradykinin receptor Bradykinin receptor B1, B2 are two main B2 receptors in mediating the protective effect of IPC