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A mathematical model of cerebral blood flow control in anaemia and hypoxia

机译:贫血和缺氧中脑血流量控制的数学模型

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Key points The control of cerebral blood flow in hypoxia, anaemia and hypocapnia is reviewed with an emphasis on the links between cerebral blood flow and possible stimuli. A mathematical model is developed to examine the changes in the partial pressure of oxygen in brain tissue associated with changes in cerebral blood flow regulation produced by carbon dioxide, anaemia and hypoxia. The model demonstrates that hypoxia, anaemia and hypocapnia, alone or in combination, produce varying degrees of cerebral hypoxia, an effect exacerbated when blood flow regulation is impaired. The suitability of brain hypoxia as a common regulator of cerebral blood flow in hypoxia and anaemia was explored, although we failed to find support for this hypothesis. Rather, cerebral blood flow appears to be related to arterial oxygen concentration in both anaemia and hypoxia. Abstract A mathematical model is developed to examine the changes in the partial pressure of oxygen in brain tissue associated with changes in cerebral blood flow regulation produced by carbon dioxide, anaemia and hypoxia. The model simulation assesses the physiological plausibility of some currently hypothesized cerebral blood flow control mechanisms in hypoxia and anaemia, and also examines the impact of anaemia and hypoxia on brain hypoxia. In addition, carbon dioxide is examined for its impact on brain hypoxia in the context of concomitant changes associated with anaemia and hypoxia. The model calculations are based on a single compartment of brain tissue with constant metabolism and perfusion pressure, as well as previously developed equations describing oxygen and carbon dioxide carriage in blood. Experimental data are used to develop the control equations for cerebral blood flow regulation. The interactive model illustrates that there are clear interactions of anaemia, hypoxia and carbon dioxide in the determination of cerebral blood flow and brain tissue oxygen tension. In both anaemia and hypoxia, cerebral blood flow increases to maintain oxygen delivery, with brain hypoxia increasing when cerebral blood flow control mechanisms are impaired. Hypocapnia superimposes its effects, increasing brain hypoxia. Hypoxia, anaemia and hypocapnia, alone or in combination, produce varying degrees of cerebral hypoxia, and this effect is exacerbated when blood flow regulation is degraded by conditions that negatively impact cerebrovascular control. Differences in brain hypoxia in anaemia and hypoxia suggest that brain oxygen tension is not a plausible sensor for cerebral blood flow control.
机译:重点指导缺氧,贫血和缺钙中的脑血流量的控制是重点探讨脑血流与可能刺激之间的联系。开发了数学模型,以检查与二氧化碳,贫血和缺氧产生的脑血流量调节变化相关的脑组织中氧组织中氧气分压的变化。该模型表明,缺氧,贫血和丘脑,单独或组合,产生不同程度的脑缺氧,当血流调节受损时,效果加剧。探讨了脑缺氧作为缺氧和贫血中脑血流量的常见调节剂,虽然我们未能找到对这一假设的支持。相反,脑血流似乎与贫血和缺氧中的动脉氧浓度有关。摘要开发了一种数学模型,以检查脑组织中氧气部分压力的变化,与二氧化碳,贫血和缺氧产生的脑血流量调节变化相关。模型模拟评估了一些目前缺氧和贫血中一些目前假设的脑血流量控制机制的生理合理性,并检查了贫血和缺氧对脑缺氧的影响。此外,在与贫血和缺氧相关的伴随变化的情况下,检查二氧化碳对脑缺氧的影响。模型计算基于脑组织的单个隔间,具有恒定的代谢和灌注压力,以及先前显得的等式描述血液中的氧气和二氧化碳托架。实验数据用于开发用于脑血流调节的控制方程。互动模型说明了贫血,缺氧和二氧化碳的清晰相互作用在测定脑血流量和脑组织氧气张力中。在贫血和缺氧中,脑血流量增加以维持氧递送,随着脑血流控制机制受损时,脑缺氧增加。丘脑疹叠加其效果,增加脑缺氧。缺氧,贫血和胚乳,单独或组合,产生不同程度的脑缺氧,当血流调节因累积脑血管控制的条件降解时,这种效果加剧了这种效果。贫血和缺氧中脑缺氧的差异表明,脑氧张力不是脑血流量控制的可粘性传感器。

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