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目的探讨心血管系统压力负荷增加到心肌肥厚形成的过程中血清中肿瘤坏死因子-α(TNF-α)、白介素-1β(IL-β)、白介素-6(IL-6)等细胞因子的变化及意义。方法腹主动脉部分缩窄制备心肌肥厚动物模型。用鼠尾动脉测压仪测定动物不同时间点的动脉血压;用放免法检测血清TNF-α、IL-1β和IL-6的浓度;用电子天平称量左心室重;计算心重指数(左心重mg/体质量g)。结果与对照组相比,实验组第3天高血压形成(P<0.01),1周后血压继续升高并稳定在一定水平(P<0.01);而心重指数在第3天未见明显差异,1周开始出现差异,此后逐渐加重,分别为(P<0.05)和(P<0.01);血清TNF-α第1周已经升高(P<0.05)、IL-1β、IL-6至第2周升高(P<0.01),且与心肌肥厚程度正相关(P<0.01)。结论细胞因子可能参与了压力超负荷性心肌肥厚的发生和发展。
Objective To investigate the changes of serum cytokines such as TNF-α, IL-β, IL-6 during the process of cardiovascular system stress load increase to the formation of cardiac hypertrophy And meaning. Methods Abdominal aorta was partially narrowed to make animal model of cardiac hypertrophy. Rat arterial blood pressure was measured at different time points by rat tail arterial manometer; serum TNF-α, IL-1β and IL-6 concentrations were measured by radioimmunoassay; left ventricular mass was measured by electronic balance; mg / body weight g). Results Compared with the control group, the experimental group formed hypertension on the third day (P <0.01), and the blood pressure continued to increase and stabilized at a certain level one week later (P <0.01); while the index of cardiac function did not show significant difference on the third day (P <0.05) and (P <0.01) respectively. The levels of serum TNF-α in the first week had been increased (P <0.05). The levels of IL-1β, IL-6 and 2 weeks (P <0.01), and positively correlated with the degree of myocardial hypertrophy (P <0.01). Conclusion Cytokines may be involved in the occurrence and development of stress overload myocardial hypertrophy.