慢性心力衰竭大鼠模型TNF-α、IFN-γ、IL-4和IL-10的表达

目的：检测慢性心力衰竭病程肿瘤坏死因子α（tumor necrosis factorα,TNF-α）、干扰素-γ（inter-feron-γ,IFN-γ）、白细胞介素-4（interleukin-4,IL-4）和白细胞介素-10（interleukin-10,IL-10）水平的动态变化,以期探讨慢性心力衰竭过程免疫系统状况变化。方法：采用纯种Wistar大鼠作为实验动物,分为正常对照组、假手术组和模型组,每个亚组均10只。采用腹主动脉结扎方法制作慢性心力衰竭模型。术后每两周行超声心动图、血液动力学检测,并取静脉血放射免疫分析进行TNF-α、IFN-γ、IL-4和IL-10的检测。结果：腹主动脉结扎后3月内是心功能代偿期,6月时是心功能失代偿期。在心力衰竭进程中,TNF-α和IFN-γ先降低后升高,IL-4和IL-10水平先升高后降低。结论：心力衰竭的不同进程,免疫机制发生变化,心功能代偿期以体液免疫为主,心功能失代偿期以细胞免疫为主。

Serum Expression of Cytokines TNF-α, IFN-γ, IL-4 and IL-10 in Rat Models of Chronic Heart Failure

Objective To study the changes of immuno - status in the course of chronic heart failure in rat models with investigating the serum expression of cytokines TNF-α, IFN-γ, IL - 4 and IL - 10. Methods Wistar rat models of chronic heart failure were prepared with constriction of abdominal aorta. Anatomic （with ultrasound） and hemodynamic （with cardiac catheterization） pa- rameters of cardiac function were examined every 2 weeks until 6 months after establishment of the models. At the same time, serum expression of TNF-α, IFN-γ IL -4 and IL - 10 were determined with RIA. Same examinations were pertormed on non -intervened control rats and sham -operated （ dissection around the abdominal aorta only） control rats as well. Results Up to 3rd month after establishment of the models, the model rats demonstrated impaired cardiac function but remained compensated. By 6^th month, frank cardiac failure was demonstrated by all criteria. Serum TNF-α,and IFN-γ levels in the models were significantly lower than those in the 2 control groups by 3^nd month. But were significantly higher than those in the controls by 6^th month. Conversely, serum IL -4 and IL - 10 levels were significantly higher in the models by 3^nd month, but became significantly lower than those in controls by 6^th month （ all P 〈 0.01 ）. Conclusion Marked change of immuno - mechanism trok place through the course of development of cardiac failure in the model rats. In the early compencated stage （ 1^nd 3 months）, humoral immune mechanism played chief role, but in the decompensated stage, cellular immune mechanism was dominant.