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首页> 外文期刊>American Journal of Physiology >Interaction among autoregulation, CO2 reactivity, and intracranial pressure: a mathematical model.
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Interaction among autoregulation, CO2 reactivity, and intracranial pressure: a mathematical model.

机译:自动调节,CO2反应性和颅内压之间的相互作用:数学模型。

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The relationships among cerebral blood flow, cerebral blood volume, intracranial pressure (ICP), and the action of cerebrovascular regulatory mechanisms (autoregulation and CO2 reactivity) were investigated by means of a mathematical model. The model incorporates the cerebrospinal fluid (CSF) circulation, the intracranial pressure-volume relationship, and cerebral hemodynamics. The latter is based on the following main assumptions: the middle cerebral arteries behave passively following transmural pressure changes; the pial arterial circulation includes two segments (large and small pial arteries) subject to different autoregulation mechanisms; and the venous cerebrovascular bed behaves as a Starling resistor. A new aspect of the model exists in the description of CO2 reactivity in the pial arterial circulation and in the analysis of its nonlinear interaction with autoregulation. Simulation results, obtained at constant ICP using various combinations of mean arterial pressure and CO2 pressure, substantially support data on cerebral blood flow and velocity reported in the physiological literature concerning both the separate effects of CO2 and autoregulation and their nonlinear interaction. Simulations performed in dynamic conditions with varying ICP underline the existence of a significant correlation between ICP dynamics and cerebral hemodynamics in response to CO2 changes. This correlation may significantly increase in pathological subjects with poor intracranial compliance and reduced CSF outflow. In perspective, the model can be used to study ICP and blood velocity time patterns in neurosurgical patients in order to gain a deeper insight into the pathophysiological mechanisms leading to intracranial hypertension and secondary brain damage.
机译:通过数学模型研究了脑血流量,脑血容量,颅内压(ICP)和脑血管调节机制(自动调节和CO2反应性)的作用之间的关系。该模型结合了脑脊液(CSF)循环,颅内压力-体积关系和脑血流动力学。后者基于以下主要假设:大脑中动脉在透壁压力变化后被动活动。颈动脉循环包括受不同自动调节机制影响的两个部分(大和小颈动脉)。静脉脑血管床表现为Starling电阻器。该模型的一个新方面存在于描述部分动脉循环中的CO2反应性以及分析其与自动调节的非线性相互作用中。使用平均动脉压和CO2压力的各种组合在恒定ICP下获得的模拟结果,基本上支持了生理文献中报道的有关CO2和自动调节的单独作用及其非线性相互作用的脑血流量和速度数据。在动态条件下使用变化的ICP进行的仿真强调了ICP动力学与响应CO2变化的脑血流动力学之间存在显着相关性。这种相关性在颅内顺应性差和脑脊液流出减少的病理受试者中可能会显着增加。从角度来看,该模型可用于研究神经外科患者的ICP和血流速度时间模式,以便更深入地了解导致颅内高压和继发性脑损伤的病理生理机制。

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