摘要
心肌缺血预适应 (IPC)是一种很强的机体内源性保护机制。存在早期保护和延迟保护双峰 ,早期保护在IPC后 1～ 3小时消失 ,而延迟保护在IPC 2 4小时后可重新出现。两者作用机制不完全相同 ,延迟保护主要通过信号转导通路的激活 ,增加细胞内保护蛋白合成起效。因其较宽的保护作用时间窗 。
Ischemic preconditioning is an endogenous protective mechanism which occurs in two distinct temporal phases: early preconditioning and delayed preconditioning. The former develops almost immediately and disappears within 1～3 hours, while the latter begins 24h after the ischemic stimulus. Increased protein synthesis induces delayed cardioprotective effect by activation of signaling pathway. It is indicated that delayed preconditioning might have potential clinical application because of the wide protective time window.
出处
《心血管病学进展》
CAS
2003年第2期92-96,共5页
Advances in Cardiovascular Diseases
关键词
延迟预适应
缺血再灌注损伤
信号转导通路
delayed preconditioning ischemic/reperfusion injury cascade of signaling events
