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非呼吸性酸中毒时外周和中枢化学敏感机制在脑内细胞外pH值调控中的协同作用。

Cooperation of peripheral and central chemosensitive mechanisms in the control of the extracellular pH in brain in non-respiratory acidosis.

作者信息

Middendorf T, Loeschcke H H

出版信息

Pflugers Arch. 1978 Aug;375(3):257-60. doi: 10.1007/BF00582439.

Abstract

The mathematical model of the respiratory control system in man of Middendorf and Loeschcke (1976 a, b) opens the possibility to stimulate the constellation of parameters in non-respiratory acidosis. Several investigators agree that the pH in CSF or in the extracellular fluid of the brain stays remarkably constant in this situation and it can be shown that this is a result of a precise control rather than the consequence of a sluggishly reacting system. Application of the model assuming constant extracellular brain pH allowed to calculate the relative sensitivities to pH changes of the central and the peripheral sensory mechanisms generating respiratory drive. Assuming air breathing and a normal critical arterial O2-pressure and otherwise normal parameters of respiration, circulation and blood composition (except diminished buffer base) the central chemosensitivity to a pH change turned out to be 25 times the peripheral. This factor is critically dependent on the ratio of the bicarbonate change in extracellular brain fluid to that in arterial blood. The coinciding data of Fencl (1971) and of Kronenberg and Cain (1968) were used for the calculation.

摘要

米登多夫和勒施克(1976年a,b)提出的人体呼吸控制系统数学模型,为刺激非呼吸性酸中毒中的参数组合提供了可能性。几位研究者一致认为,在这种情况下,脑脊液或大脑细胞外液中的pH值保持相当恒定,并且可以证明这是精确控制的结果,而不是反应迟缓的系统的结果。应用假设大脑细胞外pH值恒定的模型,可以计算出产生呼吸驱动的中枢和外周感觉机制对pH变化的相对敏感性。假设进行空气呼吸、动脉血氧分压正常且呼吸、循环和血液成分的其他参数正常(缓冲碱减少除外),结果表明中枢对pH变化的化学敏感性是外周的25倍。这个因素严重依赖于大脑细胞外液中碳酸氢盐变化与动脉血中碳酸氢盐变化的比率。计算时使用了芬克尔(1971年)以及克罗嫩贝格和凯恩(1968年)的一致数据。

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