心肌缺血/再灌注损伤与炎症反应

摘要/Abstract

摘要： 动物实验及临床研究均支持炎症反应参与了心肌缺血/再灌注损伤的过程, 但炎症本身及其对心肌缺血/再灌注损伤的影响相当复杂。心肌缺血/再灌注后, 在缺血损伤区有多种细胞因子表达及炎细胞浸润, 构成了缺血再灌注损伤向炎症性损伤转变的基础。本文对几种炎症反应中的细胞因子、炎症细胞、花生四烯酸代谢产物及环氧合酶等在心肌缺血再灌注中的作用作一综述。

关键词: 缺血再灌注, 细胞因子, 炎症细胞, 花生四烯酸代谢产物, 环氧合酶

Abstract: In both clinical and animal experiments, it has been confirmed that the inflammation in heart is involved in the development of heart injury after the ischemia/reperfusion. However, the pro-inflammatory mechanism is extremely complicated. Recently, a growing number of reports indicates that many factors play their roles in the inflammation, such as cytokinemia, inflammatory cells, metabolic product of arachidonic acid and COX et al. They are released/presented in the region of myocardial ischemia/reperfusion and include both ischemic and secondary heart injury.

Key words: ischemic/reperfusion, cytokinemia, inflammatory cell, metabolic product of arachidonic acid, cycloxygenase

中图分类号:

R965

董六一, 陈志武. 心肌缺血/再灌注损伤与炎症反应[J]. 中国临床药理学与治疗学, 2008, 13(5): 582-588.

DONG Liu-yi, CHEN Zhi-wu. Myocardial ischemia/reperfusion injury and inflammatory reaction[J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2008, 13(5): 582-588.

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