医学
缺血
心肌再灌注损伤
心肌缺血
内科学
心脏病学
出处
期刊:Circulation
[Ovid Technologies (Wolters Kluwer)]
日期:1995-03-15
卷期号:91 (6): 1872-1885
被引量:428
标识
DOI:10.1161/01.cir.91.6.1872
摘要
In the intact organism, ischemic myocardial injury initiates an acute inflammatory response in which polymorphonuclear leukocytes (PMNs) are major participants. Evidence indicates that the interplaying inflammatory reactions are augmented by reperfusion and that accumulating PMNs can contribute to myocardial damage, eg, by release of oxygen-derived free radicals, proteases, and leukotrienes. In experimental models, interventions aimed at PMN inhibition can exert cardioprotective effects, and some of these strategies raise hope for future clinical applications. A greater understanding of the mechanisms involved in PMN-mediated myocardial damage is necessary for designing a rational approach to reduce the putative detrimental effects of PMNs without antagonizing their favorable consequences in tissue healing.
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