An analytical model for axial diffusion in the Krogh cylinder.
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Biomedical subjects
Publications and source records attributed to D D Reneau.
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The rate of oxygen disappearance from the gerbil cerebral cortex was measured during bilateral carotid artery occlusion with an oxygen microelectrode at normal tissue PO2 and under hyperbaric oxygenation. The oxygen disappearance rate (ODR) was found to be heavily dependent on the PO2 at occlusion due to the desaturation of hemoglobin-bound oxygen. When the tissue PO2 was elevated to a level high enough to saturate hemoglobin, the ODR reflected the oxygen consumption rate which was calculated to range from 1.6-7.4 cc O2/100 cc tissue-min. for ten barbiturate-anesthetized animals. The fall in PO2 was found not to be totally linear to zero in many cases, but instead consisted of a linear phase followed by a period of decreasing slope. We believe this phase of changing slope represents a diminishing oxygen consumption rate. The exact nature of this decrease is not known but perhaps is an inhibitory response to the accumulation of metabolites as a result of the circulation arrest.
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Based on the results obtained in this study and the results of others it seems safe to conclude the following: 1) Fetal brain PO2 values are considerably lower than those found in adult brain. 2) Administration of 100% oxygen to the mother can (but not always) significantly raise the PO2 at a specific point in the fetal cortex. 3) The response of fetal brain PO2 to changes in maternal arterial PO2 is delayed by a finite quantity of time of the order of magnitude of 38 seconds. 4) The time required for the fetal brain PO2 to reach a minimum following a decrease in the PO2 of maternal arterial blood coincides closely with the time required for the maternal arterial PO2 to reach its minimum plus the pure transport delay time (38 seconds). 5) The fetus has available a control mechanism which acts to compensate for periods of reduced PO2 in the microenvironment of the fetal cortex.
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1. A new, 2 mu tip, oxygen micro-electrode and a constantly circulated Beckman oxygen gas analyser were used to measure tissue and blood P(O) (2) in anaesthetized, curarized cats under positive pressure breathing. As a parameter for the ability of the circulation to oxygenate tissue, the ;reoxygenation time' (defined as the time required to reach the previous P(O) (2) level after a short period of anoxic anoxia) was determined on blood and cerebral cortex.2. First, it was found that haemorrhage (from 15-25 c.c./kg) alone or haemorrhage combined with sludging of the blood (by the I.V. administration of high molecular weight Dextran, 1 g/kg) markedly diminished P(O) (2) levels in blood and tissue.3. Further, the reoxygenation time was significantly affected by these procedures. Sludging markedly prolonged the reoxygenation time, an effect counteracted by the use of an anti-adhesive drug breaking up the red cell aggregates.4. Bleeding prolonged the reoxygenation time up to four times that found in the same animals previous to the bleeding.
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