Chen Shuzhen, Zhang Shaowen, Gong Yuexian, Dai Kaiyong, Sui Meirong, Yu Yi, Ning Gangmin
Department of Biomedical Engineering, Zhejiang University (Yuquan Campus), Zheda Road 38, 310027 Hangzhou, People's Republic of China.
Physiol Meas. 2008 Apr;29(4):473-95. doi: 10.1088/0967-3334/29/4/005. Epub 2008 Apr 9.
A bond graph model of the cardiovascular system with embedded autonomic nervous regulation was developed for a better understanding of the role of the autonomic nervous system (ANS) in hypertension. The model is described by a pump model of the heart and a detailed representation of the head and neck, pulmonary, coronary, abdomen and extremity circulation. It responds to sympathetic and parasympathetic activities by modifying systemic peripheral vascular resistance, heart rate, ventricular end-systolic elastance and venous unstressed volumes. The impairment of ANS is represented by an elevation of the baroreflex set point. The simulation results show that, compared with normotensive, in hypertension the systolic and diastolic blood pressure (SBP/DBP) rose from 112/77 mmHg to 144/94 mmHg and the left ventricular wall thickness (LVWT) increased from 10 mm to 12.74 mm. In the case that ANS regulation was absent, both the SBP and DBP further increased by 8 mmHg and the LVWT increased to 13.22 mm. The results also demonstrate that when ANS regulation is not severely damaged, e.g. the baroreflex set point is 97 mmHg, it still has an effect in preventing the rapid rise of blood pressure in hypertension; however, with the worsening of ANS regulation, its protective role weakens. The results agree with human physiological and pathological features in hemodynamic parameters and carotid baroreflex function curves, and indicate the role of ANS in blood pressure regulation and heart protection. In conclusion, the present model may provide a valid approach to study the pathophysiological conditions of the cardiovascular system and the mechanism of ANS regulation.
为了更好地理解自主神经系统（ANS）在高血压中的作用，开发了一种具有嵌入式自主神经调节的心血管系统键合图模型。该模型由心脏泵模型以及头部和颈部、肺部、冠状动脉、腹部和四肢循环的详细表示来描述。它通过改变全身外周血管阻力、心率、心室收缩末期弹性和静脉无应力容积来响应交感神经和副交感神经活动。ANS的损害表现为压力反射设定点升高。模拟结果表明，与血压正常者相比，高血压患者的收缩压和舒张压（SBP/DBP）从112/77 mmHg升至144/94 mmHg，左心室壁厚度（LVWT）从10 mm增加到12.74 mm。在没有ANS调节的情况下，SBP和DBP均进一步升高8 mmHg，LVWT增加到13.22 mm。结果还表明，当ANS调节未受到严重损害时，例如压力反射设定点为97 mmHg，它在预防高血压患者血压快速升高方面仍有作用；然而，随着ANS调节的恶化，其保护作用减弱。这些结果与人体血液动力学参数和颈动脉压力反射功能曲线的生理和病理特征相符，并表明了ANS在血压调节和心脏保护中的作用。总之，本模型可能为研究心血管系统的病理生理状况和ANS调节机制提供一种有效的方法。
