Marx N, Neumann F J, Ott I, Gawaz M, Koch W, Pinkau T, Schömig A
Deutsches Herzzentrum und 1. Medizinische Klinik, Technische Universität München, Germany.
J Am Coll Cardiol. 1997 Jul;30(1):165-70. doi: 10.1016/s0735-1097(97)00116-2.
This study sought to investigate whether cytokine expression in leukocytes may be induced by plasma from the reperfused heart of patients with an acute myocardial infarction (MI).
Reperfusion in acute MI is associated with deleterious local and systemic inflammatory responses that are regulated by cytokines. Induction of cytokine expression in resident leukocytes could contribute to inflammatory responses of the ischemic and reperfused heart.
Blood samples of 10 patients with an acute MI were obtained simultaneously from the coronary sinus and the aorta before and 5 min after recanalization of the coronary occlusion. Ten patients with elective percutaneous transluminal coronary angioplasty served as a control group. We incubated leukocytes from healthy donors with plasma samples and analyzed mRNA expression of interleukin (IL)-1 beta, IL-6, IL-8 and tumor necrosis factor-alpha (TNF-alpha) by Northern blot analysis.
In patients with an acute MI, plasma obtained from the coronary sinus after recanalization increased the mRNA expression of IL-1 beta and IL-8 compared with that of plasma before recanalization (median [quartiles] difference before vs. after recanalization: 34.5 [4, 137], p = 0.017, for IL-1 beta; 18.5 [4, 35], p = 0.032, for IL-8) and simultaneously obtained aortic plasma (median [quartiles] coronary sinus-aortic differences after recanalization: 45.5 [-3, 115], p = 0.021, for IL-1 beta; 16 [4, 52], p = 0.005, for IL-8). No induction of IL-6 and TNF-alpha expression could be observed. No changes found in the study patients were detectable in the control group.
Plasma from the ischemic and reperfused heart stimulates the expression of IL-1 beta and IL-8 in leukocytes. Therefore, leukocyte-derived cytokines may contribute to the regulation of cardiac inflammatory responses in patients with an acute MI.
本研究旨在探究急性心肌梗死(MI)患者再灌注心脏的血浆是否可诱导白细胞中的细胞因子表达。
急性MI再灌注与由细胞因子调节的有害局部和全身炎症反应相关。驻留白细胞中细胞因子表达的诱导可能有助于缺血和再灌注心脏的炎症反应。
在10例急性MI患者冠状动脉闭塞再通前及再通后5分钟,同时从冠状窦和主动脉采集血样。10例行择期经皮腔内冠状动脉成形术的患者作为对照组。我们将健康供体的白细胞与血浆样本孵育,并通过Northern印迹分析检测白细胞介素(IL)-1β、IL-6、IL-8和肿瘤坏死因子-α(TNF-α)的mRNA表达。
急性MI患者再通后从冠状窦获取的血浆与再通前相比,IL-1β和IL-8的mRNA表达增加(再通前与再通后中位数[四分位数间距]差异:IL-1β为34.5[4, 137],p = 0.017;IL-8为18.5[4, 35],p = 0.032),同时获取的主动脉血浆也有此变化(再通后冠状窦 - 主动脉中位数[四分位数间距]差异:IL-1β为45.5[-3, 115],p = 0.021;IL-8为16[4, 52],p = 0.005)。未观察到IL-6和TNF-α表达的诱导。对照组未发现研究患者中出现的变化。
缺血和再灌注心脏的血浆刺激白细胞中IL-1β和IL-8的表达。因此,白细胞衍生的细胞因子可能有助于调节急性MI患者的心脏炎症反应。