首页> 外文会议>1995 IEEE engineering in medicine and biology 17th annual conference and 21st Canadian medical and biological engineering conference >A model of the autonomic control of heart rate at the pacemaker cell level through G-proteins
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A model of the autonomic control of heart rate at the pacemaker cell level through G-proteins

机译:通过G蛋白在起搏器细胞水平上自主控制心率的模型

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A mathematical model of the pacemaker cell of the mammal sinoatrial node, based upon the Yanagihara-Noma-Irisawa equations, is presented here. Its aim is to mimic the control of the pacemaker cell, as measured on the resulting heart rate, by both branches of the autonomic nervous system (ANS). It is a simplification of the original model by the suppression of some variables (but no ionic current being removed). It also uses a dynamical model of the G-proteins as actuators of this control in the system, and a construction of the sympathetic and vagal impulses, reflecting respiratory sinus arrhythmia and baroreflex influence. These characteristics make it a model compatible with what is known of the electrophysiological mechanisms of pacemak-ing at the single cell level, and with the observed spectral characteristics of short-term (respiratory) heart rate variability at the whole heart (electrocardiographic) level, thus partly bridging a gap between these two representation levels of the ANS.
机译:本文介绍了基于Yanagihara-Noma-Irisawa方程的哺乳动物窦房结起搏器细胞的数学模型。它的目的是模仿自主神经系统(ANS)的两个分支对起搏器细胞的控制,该控制是根据产生的心率来进行的。通过抑制某些变量(但没有消除离子电流)简化了原始模型。它还使用了G蛋白的动力学模型作为系统中该控制的执行器,并构建了交感和迷走神经冲动,反映了呼吸窦性心律不齐和压力反射反射的影响。这些特征使其成为一个模型,该模型与已知的单细胞水平起搏的电生理机制,以及所观察到的整个心脏(心电图)水平的短期(呼吸)心率变异性的光谱特征兼容,因此,部分弥补了这两个ANS表示级别之间的差距。

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