Niederbichler Andreas D, Papst Stephan, Claassen Leif, Jokuszies Andreas, Ipaktchi Kyros, Reimers Kerstin, Hirsch Tobias, Steinstraesser Lars, Kraft Theresia, Vogt Peter M
Eplasty. 2010 Jun 21;10:e45.
Many studies have demonstrated the existence of an anti-inflammatory, parasympathetic pathway, termed as the inflammatory reflex. Burn-induced heart failure has been investigated in many previous studies. Proinflammatory cytokines, such as TNF-alpha, IL-1beta, and IL-6, have been shown to play a key pathogenetic role and vagus nerve stimulation attenuates proinflammatory cytokine production. This study was designed to evaluate postburn alterations of cardiac functional parameters after vagal electrostimulation.
A 30% total body surface area standardized, full-thickness rat burn model was used. Electric stimulation of the vagus nerve was performed. The following functional cardiac parameters were measured by ventricular microcatheterization: Maximal and minimal left ventricular pressure, mean left ventricular pressure, end-diastolic pressure (EDP), positive and negative pressure rise and fall (+/-dP/dt), cardiac contractility index, and assessment of the heart rate.
Vagus nerve stimulation improved maximal and minimal left ventricular pressure values compared with burn-only animals. End-diastolic pressure was elevated significantly in stimulated animals; however, EDP values were comparable with those in sham-injured animals. Analyzing positive and negative pressure development, +/-dP/dt was restored to levels measured in sham-injured animals but not to control animal levels. No variations in heart rate were found.
We as well as others have shown that inflammation after burn injury is a key pathogenetic element, and this study provides new evidence that cardiac function is also improved by vagus nerve stimulation. These results lead us to consider novel therapeutic options for the treatment of postburn cardiac dysfunction.
许多研究已证实存在一条抗炎性副交感神经通路,称为炎症反射。此前已有多项研究对烧伤所致心力衰竭进行了调查。促炎细胞因子,如肿瘤坏死因子-α、白细胞介素-1β和白细胞介素-6,已被证明发挥关键的致病作用,而迷走神经刺激可减弱促炎细胞因子的产生。本研究旨在评估迷走神经电刺激后烧伤心脏功能参数的变化。
采用30%体表面积标准化全层大鼠烧伤模型。对迷走神经进行电刺激。通过心室微导管插入术测量以下心脏功能参数:左心室最大和最小压力、平均左心室压力、舒张末期压力(EDP)、正负压力上升和下降(+/-dP/dt)、心脏收缩指数以及心率评估。
与仅烧伤动物相比,迷走神经刺激改善了左心室最大和最小压力值。刺激动物的舒张末期压力显著升高;然而,EDP值与假损伤动物相当。分析正负压力变化时,+/-dP/dt恢复到假损伤动物测量的水平,但未恢复到对照动物水平。未发现心率有变化。
我们以及其他研究表明烧伤后的炎症是关键的致病因素,本研究提供了新的证据,即迷走神经刺激也可改善心脏功能。这些结果促使我们考虑治疗烧伤后心脏功能障碍的新治疗选择。