“缺血后处理”减轻已缺血心肌再灌注损伤

本室最近发现多次短暂复氧/停复处理可减轻已缺氧心肌细胞复氧损伤，提出“缺血后处理↖PC）”观点。本工作旨在进一步研究和确证IPC效应、分析其与心肌ONOO-形成的关系；利用清醒动物心肌缺血模型，探寻IPC最佳模式，并与缺血预处理心肌保护作用对比，探讨IPC可能的价值和临床意义，可望为缺血性心脏病的治疗提供新思路和直接依据。

The purpose of the present study was to determine the effect of ischemia postconditioning (IPC), the idea that we put forward firstly, on myocardial ischemia reperfusion (MI/R) injury and the relationship between IPC and production of peroxynitrite (ONOO－). The main results were as following..(1) We have found in a rat cardiac myocyte hypoxia/reoxygenation (H/R) model that seveval short episodes of intermittent H/R after a prolonged H pretects myocytes against reoxygenation injury and signaficanty attenuates apoptosis and increases myocyte viability. In MI/R rabbits in vivo, we demonstrated that IPC, like ischemic preconditioning (IP), exerts an anti-apoptotic effect, which may contribute partly to the reduction of myocardial infarction by IPC..(2) In an in vivo MI/R model we have demonstrated that insulin is the primary protective component of the glucose-insulin-potassium (GIK) cocktail that protects against MI/R injury, and that administration of insulin activated Akt through the PI3-kinase dependent mechanism and reduced postischemic myocardial apoptotic death. Phosphorylation of eNOS and the concurrent increase of NO production contributes significantly to the anti-apoptotic effect of insulin..(3) ONOO－ may act as a "double-edged sword" in postischemic myocardial injury. This compound is directly toxic to the cardiac tissue at a relatively high concentration, but it can indirectly protect myocardial cells from neutrophil-induced injury at a much lower concentration..