Grisham M B, Granger D N, Lefer D J
Department of Molecular and Cellular Physiology, Louisiana State University Medical Center, Shreveport 71130-3932, USA.
Free Radic Biol Med. 1998 Sep;25(4-5):404-33. doi: 10.1016/s0891-5849(98)00094-x.
Ischemia and reperfusion (I/R) are thought to play an important role in the pathophysiology of ischemic diseases of the heart. It is now well appreciated that leukocyte-endothelial cell interactions are important determinants for I/R-induced microvascular injury and dysfunction. There is a growing body of experimental data to suggest that reactive metabolites of oxygen and nitrogen are important physiological modulators of leukocyte-endothelial cell interactions. A number of investigators have demonstrated that I/R enhances oxidant production within the microcirculation resulting in increases in leukocyte adhesion and transendothelial cell migration. Several other studies have shown that exogenous nitric oxide (NO) donors may attenuate leukocyte and platelet adhesion and/or aggregation in a number of different inflammatory conditions including I/R. The objective of this review is to discuss the physiological chemistry of reactive metabolites of oxygen and nitrogen with special attention given to those interactions that may modulate leukocyte-endothelial cell interactions, provide an overview of the evidence implicating reactive metabolites of oxygen and nitrogen as modulators of leukocyte-endothelial cell interactions in vivo, and discuss how these mechanisms may be involved in the pathophysiology of ischemic heart disease.
缺血再灌注（I/R）被认为在心脏缺血性疾病的病理生理学中起重要作用。现在人们已经充分认识到，白细胞与内皮细胞的相互作用是I/R诱导的微血管损伤和功能障碍的重要决定因素。越来越多的实验数据表明，氧和氮的活性代谢产物是白细胞与内皮细胞相互作用的重要生理调节剂。许多研究人员已经证明，I/R会增强微循环内的氧化剂产生，导致白细胞黏附和跨内皮细胞迁移增加。其他一些研究表明，外源性一氧化氮（NO）供体可能会减弱包括I/R在内的多种不同炎症条件下的白细胞和血小板黏附及/或聚集。本综述的目的是讨论氧和氮的活性代谢产物的生理化学，特别关注那些可能调节白细胞与内皮细胞相互作用的相互作用，概述将氧和氮的活性代谢产物作为体内白细胞与内皮细胞相互作用调节剂的证据，并讨论这些机制如何可能参与缺血性心脏病的病理生理学。
