Mehta J, Dinerman J, Mehta P, Saldeen T G, Lawson D, Donnelly W H, Wallin R
Department of Medicine, University of Florida, College of Medicine, Gainesville 32610.
Circulation. 1989 Mar;79(3):549-56. doi: 10.1161/01.cir.79.3.549.
Neutrophils contribute to the healing of and scar formation in myocardium after ischemic injury. Many recent studies indicate that neutrophils may be involved in the genesis and propagation of myocardial ischemia. To characterize neutrophil function in ischemic heart disease, neutrophil chemotaxis, leukotriene B4 (LTB4) generation, and elastase release in plasma were measured in 20 patients with stable angina, 17 patients with unstable angina or acute myocardial infarction (AMI), and 20 age-matched control subjects. Neutrophils from patients with stable angina exhibited markedly increased chemotactic activity and LTB4 generation as compared with the age-matched control subjects (p less than 0.01). Neutrophils of nine of 17 patients with unstable angina or AMI clumped spontaneously ex vivo and exhibited marked pseudopod formation and granule extrusion on electron microscopy. Subsequent chemotactic activity and LTB4 generation by neutrophils from these patients was less than in patients with stable angina, suggesting previous in vivo activation. Plasma levels of peptide B beta, a product of fibrin degradation by human neutrophil elastase, were approximately 15-fold higher (p less than 0.001) in patients with unstable angina or AMI (588 +/- 171 pmol/l, mean +/- SEM) compared with those in patients with stable angina (37 +/- 25 pmol/l) or control subjects (40 +/- 22 pmol/l), confirming intense in vivo neutrophil activation. Our study shows enhanced neutrophil function in patients with ischemic heart disease. The increased neutrophil chemotactic activity and LTB4 generation may be markers of stable angina pectoris. Intense neutrophil activation in unstable angina or AMI, as manifested by morphologic changes in neutrophils and elastase release, may relate to ongoing in vivo cellular activation.
中性粒细胞有助于心肌缺血损伤后的愈合和瘢痕形成。最近的许多研究表明，中性粒细胞可能参与心肌缺血的发生和发展。为了明确中性粒细胞在缺血性心脏病中的功能，对20例稳定型心绞痛患者、17例不稳定型心绞痛或急性心肌梗死（AMI）患者以及20例年龄匹配的对照者进行了中性粒细胞趋化性、白三烯B4（LTB4）生成及血浆中弹性蛋白酶释放的检测。与年龄匹配的对照者相比，稳定型心绞痛患者的中性粒细胞表现出明显增强的趋化活性和LTB4生成（p<0.01）。17例不稳定型心绞痛或AMI患者中有9例的中性粒细胞在体外自发聚集，电子显微镜下可见明显的伪足形成和颗粒挤出。这些患者的中性粒细胞随后的趋化活性和LTB4生成低于稳定型心绞痛患者，提示先前在体内已被激活。与稳定型心绞痛患者（37±25 pmol/l）或对照者（40±22 pmol/l）相比，不稳定型心绞痛或AMI患者血浆中人类中性粒细胞弹性蛋白酶降解纤维蛋白的产物肽Bβ水平大约高15倍（p<0.001）（588±171 pmol/l，均值±标准误），证实体内中性粒细胞被强烈激活。我们的研究显示缺血性心脏病患者中性粒细胞功能增强。中性粒细胞趋化活性和LTB4生成增加可能是稳定型心绞痛的标志物。不稳定型心绞痛或AMI中中性粒细胞的强烈激活，表现为中性粒细胞形态改变和弹性蛋白酶释放，可能与体内持续的细胞激活有关。
