作者: JL Mehta , DY Li
DOI: 10.1016/S0008-6363(99)00132-7
关键词:
摘要: Time for primary review 32 days. The presence of inflammatory cells in the ischemic myocardial tissues has traditionally been believed to represent pathophysiologic response injury [1]. It is only recently that inflammation related pathogenesis acute coronary syndromes [2,3], reperfusion myocardium [4], restenosis after angioplasty [5–7], failure cardiac transplant [8], and chronic heart [9]. Accordingly, relationship between with atherosclerosis ischemia now an area active investigation. Accumulation polymorphonuclear leukocytes (PMN) their activation are key features reaction associated ischemia-reperfusion [3]. Experimental studies have shown influx PMNs into results tissue beyond caused by alone [10,11]. also become apparent recruitment during involves numerous mediators [3,4]. The causative role animals supported observations reduction microvascular dysfunction strategies prevent PMN either a decrease number circulating [12], or [13]. Other [14] inhibition release PMN-derived blockade adhesion molecules on [15,16] and/or endothelial [17] reduce injury. Many aspects as participant animal models reviewed recent past [16–19]. In this report, we our current understanding patients ischemia. If concept inflammation, especially accumulation activation, disease (IHD) proven, anti-inflammatory therapy may be designed treat common … * Corresponding author. Tel.: +1-352-379-4160; fax: +1-352-379-4161 mehta{at}medmac.ufl.edu