Interaction between carotid baroregulation and the pulsating heart: a mathematical model
Interaction between carotid baroregulation and the pulsating heart: a mathematical model
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DOI：
10.1152/ajpheart.1998.275.5.h1733
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发表时间：
1998-11-01
影响因子：
4.8
通讯作者：
Ursino, M
中科院分区：
文献类型：
--
作者：
Ursino, M
本文提出了一个在脉动条件下由颈动脉压力感受器控制短期动脉压的数学模型。该模型包括一个弹性变量描述的左，右心脏，全身（内脏和extrasplanchnic）和肺循环，传入颈动脉压力感受器通路，交感神经和迷走神经传出活动，和行动的几个效应机制。后一种机制响应交感神经和迷走神经作用，通过改变全身外周阻力、全身静脉无应激体积、心脏周期和收缩末期弹性来起作用。该模型被用来模拟在不同的实验中颈动脉压力感受器反射，搏动的心脏，和效应器的反应之间的相互作用。在所有情况下，模型和实验结果之间有令人满意的协议。心率控制的实验数据可以通过假设交感-副交感神经系统在心动周期上线性相互作用来解释。颈动脉压力感受性反射对心功能曲线有明显的调制作用。然而，这种效应在体内被动脉和心房压力的变化所掩盖。在心脏起搏期间，心输出量在中等心率水平下随频率增加，然后由于每搏输出量减少而无法进一步增加。颈动脉窦从非搏动性灌注转变为搏动性灌注降低了整体压力感受器反射增益，并显著改变了颈动脉压力感受器反射的操作。最后，敏感性分析表明，静脉无应力容量控制在急性出血的早期血流动力学反应中起主要作用，而全身阻力和心率控制则不太重要。
A mathematical model of short-term arterial pressure control by the carotid baroreceptors in pulsatile conditions is presented. The model includes an elastance variable description of the left and right heart, the systemic (splanchnic and extrasplanchnic) and pulmonary circulations, the afferent carotid baroreceptor pathway, the sympathetic and vagal efferent activities, and the action of several effector mechanisms. The latter mechanisms work, in response to sympathetic and vagal action, by modifying systemic peripheral resistances, systemic venous unstressed volumes, heart period, and end-systolic elastances. The model is used to simulate the interaction among the carotid baroreflex, the pulsating heart, and the effector responses in different experiments. In all cases, there has been satisfactory agreement between model and experimental results. Experimental data on heart rate control can be explained fairly well by assuming that the sympathetic-parasympathetic systems interact linearly on the heart period. The carotid baroreflex can significantly modulate the cardiac function curve. However, this effect is masked in vivo by changes in arterial and atrial pressures. During heart pacing, cardiac output increases with frequency at moderate levels of heart rate and then fails to increase further because of a reduction in stroke volume. Shifting from nonpulsatile to pulsatile perfusion of the carotid sinuses decreases the overall baroreflex gain and significantly modifies operation of the carotid baroreflex. Finally, a sensitivity analysis suggests that venous unstressed volume control plays the major role in the early hemodynamic response to acute hemorrhage, whereas systemic resistance and heart rate controls are a little less important.