肿瘤坏死因子-α对心脏交感神经节的影响

Effects of tumor necrosis factor-αon cardiac sympathetic ganglion

目的探究肿瘤坏死因子-α(TNF-α)对心脏交感神经节的影响。方法 14只成年犬随机分为两组:实验组7只,将0.1ml TNF-α(0.1mg/ml)分别局部微量注射进入左侧心脏交感神经节(LSG)、右侧心脏交感神经节(RSG);对照组7只,将同等量的生理盐水分别局部微量注射进入LSG和RSG。电压递增式高频电刺激(频率20Hz,脉宽0.1ms)作用于LSG、RSG可分别引起血压升高、心率加快,以最大收缩压(SBP)改变代表LSG功能,以心率变化代表RSG功能。微电极固定在LSG、RSG之后,使用labChart Pro软件记录并分析神经活性的频率和振幅。分别记录基础状态和干预30min后LSG、RSG的神经功能和活性。结果与基础状态相比,实验组30min后LSG和RSG功能及神经活性显著升高(P<0.05),而对照组以上指标未见显著性改变(P>0.05)。30min后,实验组LSG、RSG功能和神经活性均明显高于对照组(P<0.05)。结论 TNF-α可显著增强心脏交感神经节的功能和活性。

Objective To investigate the effects of tumor necrosis factor-α （TNF-α） on cardiac sympathetic gan- glion. Methods Fourteen adult dogs were randomly divided into two groups. In the experimental group （n= 7）, 0.1 ml TNF-a （0.1mg/ml） was microinjected into left （LSG） and right （RSG） cardiac sympathetic ganglion. The e- quivalent 0.9% saline was microinjected into LSG and RSG in control group （n = 7）. The maximum systolic blood pressure changes induced by the voltage incremental high frequency electrical stimulation （HFS： 20Hz in frequency, 0.1ms in pulse width） on LSG were measured to reflect the function status of I.SG. The heart rate changes induced by HFS on RSG were measured to reflect the function status of RSG. After the microelectrodes were immobilized on the LSG and RSG, the frequency and amplitude of neural activity were recorded and analyzed using labChart Pro software. The function and neural activity of LSG and RSG were determined at baseline and 30 minutes after TNF-α saline microinjection. Results In the experiment group, both the function and neural activity of LSG and RSG were significantly increased after 30 rain of TNF-α microinjection （P 〈0.05）. However, these parameters were not changed after microinjection of 30 min in the control group （P〉0.05）. In addition, 30 rain after TNF-α or saline microinjection, both the function and neural activity of LSG and RSG in experiment group were significantly higher than that of control group. Conclusion TNF-α could significantly enhance the neural activity and function of car- diac sympathetic ganglion.