Deng M C, Roeder N, Plenz G, Erren M, Brisse B, Soeparwata R, Scheld H H
Klinik und Poliklinik für Thorax-, Herz- und Gefässchirurgie, Westfälische Wilhelms-Universität Münster.
Z Kardiol. 1997 Oct;86(10):788-802. doi: 10.1007/s003920050117.
In situations of depressed myocardial function, the role of immunological mechanisms has been studied recently. In different pathophysiological situations, such as chronic heart failure, open heart surgery with extracorporal circulation, cardiac transplantation, myocardial infarction and angina pectoris, patterns have been described with elevation of proinflammatory cytokines, such as tumor necrosis factor-alpha, interleukin-1, interleukin-6, and reversible myocardial dysfunction, which may represent a final common pathway. The available data suggest a modulation of important determinants of pump function, i.e., contractility, preload, afterload, and heart rate, by cytokines. Potential mechanisms include the beta-adrenoceptor- and nitric oxide pathway, as well as a direct impact on intracellular calcium homeostasis. Interventional strategies based on this understanding are beginning to emerge.
在心肌功能减退的情况下，免疫机制的作用最近已得到研究。在不同的病理生理情况下，如慢性心力衰竭、体外循环心脏直视手术、心脏移植、心肌梗死和心绞痛，已发现促炎细胞因子如肿瘤坏死因子-α、白细胞介素-1、白细胞介素-6升高以及可逆性心肌功能障碍的模式，这可能代表了最终的共同途径。现有数据表明细胞因子可调节泵功能的重要决定因素，即收缩性、前负荷、后负荷和心率。潜在机制包括β-肾上腺素能受体和一氧化氮途径，以及对细胞内钙稳态的直接影响。基于这一认识的干预策略已开始出现。
