Hyder F, Shulman R G, Rothman D L
Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, Connecticut 06510, USA.
J Appl Physiol (1985). 1998 Aug;85(2):554-64. doi: 10.1152/jappl.1998.85.2.554.
On the basis of the assumption that oxygen delivery across the endothelium is proportional to capillary plasma PO2, a model is presented that links cerebral metabolic rate of oxygen utilization (CMRO2) to cerebral blood flow (CBF) through an effective diffusivity for oxygen (D) of the capillary bed. On the basis of in vivo evidence that the oxygen diffusivity properties of the capillary bed may be altered by changes in capillary PO2, hematocrit, and/or blood volume, the model allows changes in D with changes in CBF. Choice in the model of the appropriate ratio of Omega identical with (DeltaD/D)/(DeltaCBF/CBF) determines the dependence of tissue oxygen delivery on perfusion. Buxton and Frank (J. Cereb. Blood Flow. Metab. 17: 64-72, 1997) recently presented a limiting case of the present model in which Omega = 0. In contrast to the trends predicted by the model of Buxton and Frank, in the current model when Omega > 0, the proportionality between changes in CBF and CMRO2 becomes more linear, and similar degrees of proportionality can exist at different basal values of oxygen extraction fraction. The model is able to fit the observed proportionalities between CBF and CMRO2 for a large range of physiological data. Although the model does not validate any particular observed proportionality between CBF and CMRO2, generally values of (DeltaCMRO2/CMRO2)/(DeltaCBF/CBF) close to unity have been observed across ranges of graded anesthesia in rats and humans and for particular functional activations in humans. The model's capacity to fit the wide range of data indicates that the oxygen diffusivity properties of the capillary bed, which can be modified in relation to perfusion, play an important role in regulating cerebral oxygen delivery in vivo.
基于内皮细胞氧输送与毛细血管血浆氧分压成正比的假设，提出了一个模型，该模型通过毛细血管床的有效氧扩散率（D）将脑氧代谢率（CMRO2）与脑血流量（CBF）联系起来。基于体内证据，即毛细血管床的氧扩散特性可能因毛细血管氧分压、血细胞比容和/或血容量的变化而改变，该模型允许D随CBF的变化而变化。模型中适当的Ω比值（Ω = (ΔD/D)/(ΔCBF/CBF)）的选择决定了组织氧输送对灌注的依赖性。巴克斯顿和弗兰克（《脑血流与代谢杂志》17: 64 - 72, 1997）最近提出了本模型的一个极限情况，其中Ω = 0。与巴克斯顿和弗兰克模型预测的趋势相反，在当前模型中，当Ω > 0时，CBF变化与CMRO2之间的比例关系变得更加线性化，并且在不同的基础氧摄取分数值下可以存在相似程度的比例关系。该模型能够拟合大范围生理数据中观察到的CBF与CMRO2之间的比例关系。虽然该模型并未验证CBF与CMRO2之间任何特定的观察到的比例关系，但一般而言，在大鼠和人类的分级麻醉范围内以及人类的特定功能激活情况下，已观察到(ΔCMRO2/CMRO2)/(ΔCBF/CBF)的值接近1。该模型拟合广泛数据的能力表明，可根据灌注情况进行调节的毛细血管床的氧扩散特性在体内调节脑氧输送中起重要作用。
