短期动脉血压控制中多种机制相互作用的建模。

Stud Health Technol Inform. 2000;71:139-61.

A Mathematical model of the short-term arterial pressure control in humans is presented. It includes a six-compartment description of the vascular system, an elastance variable model of the pulsating heart, two groups of baroreceptors (high-pressure or sinoaortic baroreceptors and low-pressure or cardiopulmonary baroreceptors), the efferent activity in the sympathetic nerves and in the vagus, and the response of four distinct effectors (heart period, systemic peripheral resistance, systemic venous unstressed volume and heart contractility). Several experimental results reported in the physiological literature can be reproduced with the model quite well. The examples presented in this work include the effect of combined sympathetic and vagal stimulation on heart rate, the baroreflex response to mild and severe acute haemorrhages, and the baroreflex response to ventricular pacing at different rates performed during atrioventricular block. The results suggest that: i) The sympathetic nerves and the vagus interact linearly in regulating heart period. The apparent negative interaction observed experimentally can be ascribed merely to the hyperbolic relationship which links heart rate to heart period. ii) The cardiopulmonary baroafferents play a significant role in the control of systemic arterial pressure during mild haemorrhages (lower than 3-4% of the overall blood volume). In this range, they may allow arterial pressure to be maintained at its normal level without the intervention of the sinoaortic baroreceptors. In contrast, the sinoaortic baroreceptors become the major responsible of the observed cardiovascular adjustments during more severe haemorrhages, when the role of cardiopulmonary baroreceptors becomes progressively exhausted. iii) The stability margin of the closed-loop system is quite low. Increasing the static gain of the baroreceptors or reducing the rate-dependent component may result in self-sustained oscillations similar to Mayer waves.

本文提出了一种人体短期动脉血压控制的数学模型。该模型包括对血管系统的六室描述、搏动心脏的弹性变量模型、两组压力感受器（高压或窦主动脉压力感受器和低压或心肺压力感受器）、交感神经和迷走神经的传出活动，以及四种不同效应器（心动周期、全身外周阻力、全身静脉无应力容积和心脏收缩力）的反应。生理学文献中报道的几个实验结果可以用该模型很好地再现。本文给出的例子包括交感神经和迷走神经联合刺激对心率的影响、对轻度和重度急性出血的压力反射反应，以及在房室传导阻滞期间以不同速率进行心室起搏时的压力反射反应。结果表明：i）交感神经和迷走神经在调节心动周期时线性相互作用。实验中观察到的明显负相互作用仅仅可以归因于将心率与心动周期联系起来的双曲线关系。ii）心肺压力感受器传入神经在轻度出血（低于总血容量的3 - 4%）期间对全身动脉血压的控制中起重要作用。在此范围内，它们可能使动脉血压在无窦主动脉压力感受器干预的情况下维持在正常水平。相反，在更严重的出血期间，当心肺压力感受器的作用逐渐耗尽时，窦主动脉压力感受器成为观察到的心血管调节的主要负责者。iii）闭环系统的稳定裕度相当低。增加压力感受器的静态增益或降低速率依赖性成分可能导致类似于迈尔波的自持振荡。