Matsumori A, Yamada T, Suzuki H, Matoba Y, Sasayama S
Department of Internal Medicine, Faculty of Medicine, Kyoto University, Japan.
Br Heart J. 1994 Dec;72(6):561-6. doi: 10.1136/hrt.72.6.561.
To elucidate the potential role of cytokines in the pathogenesis of cardiomyopathy and myocarditis.
Experimental studies show that certain cytokines depress myocardial contractility and that tumour necrosis factor-alpha plays an important part in the pathogenesis of myocardial injury in animal models of viral and autoimmune myocarditis.
Plasma interleukin 1-alpha, interleukin 1-beta, interleukin-2, interleukin-6, tumour necrosis factor-alpha, tumour necrosis factor-beta, granulocyte-macrophage colony stimulating factor, granulocyte colony stimulating factor, macrophage colony stimulating factor, interferon-alpha and interferon-gamma were measured in 13 patients with acute myocarditis, 23 patients with dilated cardiomyopathy, 51 patients with hypertrophic cardiomyopathy, nine patients with acute myocardial infarction, 18 patients with angina pectoris, 12 patients with essential hypertension and 17 healthy controls.
Increased concentrations of cytokines were not detected in the controls. In patients with acute myocarditis, interleukin 1-alpha was detected in 23% (mean (SD) 25 (11) pg/ml), tumour necrosis factor-alpha in 46% (61 (31) pg/ml), and macrophage colony stimulating factor was 2.5 (1.8) ng/ml (normal 1.9 (0.4)). In patients with dilated cardiomyopathy, tumour necrosis factor-alpha was detected in 35% (402 (555) pg/ml). In patients with hypertrophic cardiomyopathy, interleukin-2 was detectable in 14% (2318 (4738) pg/ml) and tumour necrosis factor-alpha ws detected in 20% (992 (1517) pg/ml). The concentration of macrophage colony stimulating factor was raised in patients with acute myocardial infarction. Granulocyte colony stimulating factor was often increased in myocarditis, cardiomyopathies, acute myocardial infarction, and angina pectoris--suggesting activation of macrophages and/or endothelial cells--but this increase was not specific to these diseases. Increased concentrations of cytokines were not found in patients with essential hypertension.
These results suggest that cytokines may play a part in the pathogenesis of myocardial injury in myocarditis and cardiomyopathies and that further studies to explore the potential pathogenetic role of cytokines in myocardial diseases may be warranted.
阐明细胞因子在心肌病和心肌炎发病机制中的潜在作用。
实验研究表明，某些细胞因子可降低心肌收缩力，且肿瘤坏死因子-α在病毒性和自身免疫性心肌炎动物模型的心肌损伤发病机制中起重要作用。
检测了13例急性心肌炎患者、23例扩张型心肌病患者、51例肥厚型心肌病患者、9例急性心肌梗死患者、18例心绞痛患者、12例原发性高血压患者和17名健康对照者血浆中的白细胞介素1-α、白细胞介素1-β、白细胞介素-2、白细胞介素-6、肿瘤坏死因子-α、肿瘤坏死因子-β、粒细胞-巨噬细胞集落刺激因子、粒细胞集落刺激因子、巨噬细胞集落刺激因子、干扰素-α和干扰素-γ。
对照组未检测到细胞因子浓度升高。急性心肌炎患者中，23%检测到白细胞介素1-α（平均（标准差）25（11）pg/ml），46%检测到肿瘤坏死因子-α（61（31）pg/ml），巨噬细胞集落刺激因子为2.5（1.8）ng/ml（正常为1.9（0.4））。扩张型心肌病患者中，35%检测到肿瘤坏死因子-α（402（555）pg/ml）。肥厚型心肌病患者中，14%可检测到白细胞介素-2（2318（4738）pg/ml），20%检测到肿瘤坏死因子-α（992（1517）pg/ml）。急性心肌梗死患者巨噬细胞集落刺激因子浓度升高。粒细胞集落刺激因子在心肌炎、心肌病、急性心肌梗死和心绞痛患者中常升高，提示巨噬细胞和/或内皮细胞活化，但这种升高并非这些疾病所特有。原发性高血压患者未发现细胞因子浓度升高。
这些结果表明，细胞因子可能在心肌炎和心肌病的心肌损伤发病机制中起作用，可能有必要进一步研究以探讨细胞因子在心肌疾病中的潜在致病作用。
