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Updated: Aug 1, 2026

Cerebral Blood Oxygenation Measurement Based on Oxygen-dependent Quenching of Phosphorescence
Published on: May 4, 2011
Oxygen transport in the rat brain cortex at normobaric hyperoxia
K P Ivanov1, I B Sokolova, E P Vovenko
1I.P. Pavlov Institute of Physiology, Russian Academy of Sciences, Nab. Makarova 6, 199034 Sankt-Petersburg, Russia. kpivanov@nc2490.spb.edu
Abstract:
The distribution of oxygen tension (PO(2)) in microvessels and in the tissues of the rat brain cortex on inhaling air (normoxia) and pure oxygen at atmospheric pressure (normobaric hyperoxia) was studied with the aid of oxygen microelectrodes (diameter = 3-6 microm), under visual control using a contact optic system. At normoxia, the PO(2) of arterial blood was shown to decrease from [mean (SE)] 84.1 (1.3) mmHg in the aorta to about 60.9 (3.3) mmHg in the smallest arterioles, due to the permeability of the arteriole walls to oxygen. At normobaric hyperoxia, the PO(2) of the arterial blood decreased from 345 (6) mmHg in the aorta to 154 (11) mmHg in the smallest arterioles. In the blood of the smallest venules at normoxia and at normobaric hyperoxia, the differences between PO(2) values were smoothed out. Considerable differences between PO(2) values at normoxia and at normobaric hyperoxia were found in tissues at a distance of 10-50 microm from the arteriole walls (diameter = 10-30 microm). At hyperbaric hyperoxia these values were greater than at normoxia, by 100-150 mmHg. In the long-run, thorough measurements of PO(2) in the blood of the brain microvessels and in the tissues near to the microvessels allowed the elucidation of quantitative changes in the process of oxygen transport from the blood to the tissues after changing over from the inhalation of air to inhaling oxygen. The physiological, and possibly pathological significance of these changes requires further analysis.
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