Hasper D, Hummel M, Döcke W D, Kleber F X, Felix S B, Hetzer R, Volk H D
Institut für Medizinische Immunologie, Universitätsklinikum Charité, Berlin.
Z Kardiol. 1996 Nov;85(11):820-7.
We studied the plasma levels of TNF-alpha, IL-6, IL-8 and soluble adhesion molecules (sE-Selectin, sL-Selectin, sVCAM-1) immediately before and during mechanical circulatory support with a Biventricular Assist Device System (BVAD-"Berlin Heart") in comparison to patients with chronic heart failure (NYHA classes II/III) and patients with coronary artery disease with normal ventricular function. Additionally, the biocompatibility of the membranes used in the "Berlin Heart" was tested in vitro. IL-6 and IL-8 but not TNF-alpha could only be detected in patients with cardiogenic shock immediately before starting circulatory support. Furthermore, plasma concentrations of soluble adhesion molecules were statistically significantly elevated in patients with cardiogenic shock compared to patients with coronary artery disease. This picture of a systemic inflammatory response syndrome without significant level of TNF-alpha looks quite similar to that seen in patients following trauma and severe operations. During mechanical circulatory support plasma levels of cytokines and soluble adhesion molecules dropped to low levels in patients, who were successfully maintained on BVAD. By contrast, we have found persistently elevated levels of these mediators in patients with fatal outcome. This seems not to be the result of individual distinct response of blood cells to contact with the artificial surfaces of the device. In summary, our data suggest the development of a systemic inflammatory response syndrome may be due to hypoxia during cardiogenic shock. Persistence of systemic inflammation suggests failing of the mechanical support. Therefore, the monitoring of inflammatory mediators may be relevant as a prognostic marker in these patients (disappearance of peripheral hypoxia).
我们研究了在使用双心室辅助装置系统(BVAD - “柏林心脏”)进行机械循环支持之前及期间,与慢性心力衰竭患者(纽约心脏协会II/III级)和心室功能正常的冠心病患者相比,血浆中肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、白细胞介素-8(IL-8)和可溶性黏附分子(可溶性E-选择素、可溶性L-选择素、可溶性血管细胞黏附分子-1)的水平。此外,还在体外测试了“柏林心脏”中使用的膜的生物相容性。仅在开始循环支持前的心源性休克患者中检测到IL-6和IL-8,而未检测到TNF-α。此外,与冠心病患者相比,心源性休克患者血浆中可溶性黏附分子的浓度在统计学上显著升高。这种无显著TNF-α水平的全身炎症反应综合征的情况与创伤和重大手术后患者所见的情况非常相似。在机械循环支持期间,成功维持BVAD的患者血浆中细胞因子和可溶性黏附分子水平降至低水平。相比之下,我们发现死亡患者中这些介质水平持续升高。这似乎不是血细胞与装置人工表面接触后个体独特反应的结果。总之,我们的数据表明全身炎症反应综合征的发生可能是由于心源性休克期间的缺氧。全身炎症的持续存在表明机械支持失败。因此,监测炎症介质可能作为这些患者的预后标志物(外周缺氧的消失)具有相关性。