A physiological model for autonomic heart rate regulation in human endotoxemia.
A physiological model for autonomic heart rate regulation in human endotoxemia.
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DOI：
10.1097/shk.0b013e318200032b
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发表时间：
2011-03
期刊：
影响因子：
--
通讯作者：
Androulakis IP
中科院分区：
文献类型：
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作者：
Foteinou PT;Calvano SE;Lowry SF;Androulakis IP
全身性炎症反应综合征(SIRS)通常伴随危重疾病，可能是发病率和死亡率的重要原因。心血管功能的显著异常伴随着急性疾病，表现为持续性的快速性心律失常，这只是全身失调的一个组成部分。心脏起搏器活动受自主神经系统控制的认识促进了心率变异分析以评估自主神经活动。在急性疾病中，部分表现为副交感神经减弱的自主神经失衡与表现为SIRS表型的患者的发病率增加有关。在生物表型作为整个宿主网络元件协调作用的结果的前提下，开发了一个多尺度的人类内毒素血症模型，作为人类全身炎症的原型模型，量化了炎症和自主心率调节之间复杂关系的关键方面。在目前的研究中，心率对急性损伤的反应的变化，表现为心动过速，被模拟为反映交感神经活动过度和副交感神经衰减的自主神经失衡的结果。该模型评估了前应激对人类内毒素血症的全身炎症表现以及一系列与炎症相关的非线性情景的抗炎和心血管效应。这种建模方法提供了一个全面的概念框架，通过一个多尺度模型将炎症和生理复杂性联系起来，这可能会提高系统建模在临床研究中的翻译潜力。
The systemic inflammatory response syndrome (SIRS) often accompanies critical illnesses and can be an important cause of morbidity and mortality. Marked abnormalities in cardiovascular function accompany acute illnesses manifested as sustained tachyarrhythmias which are but one component of systemic dysregulation. The realization that cardiac pacemaker activity is under control of the autonomic nervous system has promoted the analysis of heart rate variation for assessing autonomic activities. In acute illnesses, autonomic imbalance manifesting in part as parasympathetic attenuation is associated with increased morbidity in patients who manifest SIRS phenotype. Driven by the premise that biological phenotypes emerge as the outcome of the coordinated action of network elements across the host, a multiscale model of human endotoxemia, as a prototype model of systemic inflammation in humans, is developed that quantifies critical aspects of the complex relationship between inflammation and autonomic heart rate regulation. In the present study, changes in heart rate response to acute injury, phenotypically expressed as tachycardia, are simulated as a result of autonomic imbalance that reflects sympathetic activity excess and parasympathetic attenuation. The proposed model assesses both the anti-inflammatory and cardiovascular effects of antecedent stresses upon the systemic inflammatory manifestations of human endotoxemia as well as a series of non-linear inflammatory relevant scenarios. Such a modeling approach provides a comprehensive conceptual framework linking inflammation and physiological complexity via a multiscale model that may advance the translational potential of systems modeling in clinical research.