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Updated: Mar 1, 2026

Oxygen-Glucose Deprivation and Reoxygenation as an In Vitro Ischemia-Reperfusion Injury Model for Studying Blood-Brain Barrier Dysfunction
Published on: May 7, 2015
Mathematical model of oxygen transport in the cerebral cortex
1Department of Anesthesiology, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA.ahudetz@mcw.edu
Abstract:
To estimate the magnitude of hyperemia necessary to support oxidative metabolism in the cerebral cortex during functional activation, a mathematical model of O2 transport from capillary to tissue was developed. Radial and axial gradients of O2 pressure in tissue surrounding a single capillary were calculated at normal and increased cerebral metabolic rates for O2. Cone-shaped tissue geometry and nonlinear oxyhemoglobin dissociation were assumed. Local O2 consumption was assumed to be supported with local tissue pO2 greater than 1 mmHg. The distribution of tissue pO2 was also calculated during moderate hypoxemia (paO2=42 mmHg), using experimental values of red blood cell velocity measured in individual capillaries of the rat cerebral cortex using intravital video-microscopy. The model predicted that moderate increases (=50%) in cerebral O2 consumption were supported by proportional increases in capillary blood flow. Large increases in O2 consumption (50-110%) were supported by disproportional increases in flow. During moderate hypoxemia, average tissue pO2 decreased but oxygen utilization was sustained when capillary flow was increased to a level measured in experiments. The results suggest a proportional relationship between cerebrocortical blood flow and oxygen consumption in the normal physiological range of functional activation.
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