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Ann Biomed Eng. 1997 May-Jun;25(3):565-72.

Michaelis-Menten kinetics model of oxygen consumption by rat brain slices following hypoxia.

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Department of Biomedical Engineering, Louisiana Tech University, Ruston, USA.


In the present study, we have measured partial pressure of oxygen (pO2) profiles through rat brain slices before and after periods of hypoxia (5 and 10 min) to determine its effect on tissue oxygen demand. Tissue pO2 profiles were measured through rat cerebral cortex slices superfused with phosphate buffer using oxygen (O2)-sensitive microelectrodes at different times in controls [40% O2 balance nitrogen (N2)], and at different times before and after 5 or 10 min of hypoxia (100% N2). A one-dimensional, steady-state model of ordinary diffusion with a Michaelis-Menten model of O2 consumption where the maximal O2 consumption (Vmax) and the rate at half-maximal O2 consumption (Km) were allowed to vary was used to determine the kinetics of O2 consumption. Actual pO2 profiles through tissue were fitted to theoretical profiles by a least-squares method. Vmax varied among penetrations in a control slice and among slices. Vmax seemed to decrease after hypoxic insult, but the change was not statistically significant. The Km value measured before hypoxia was lower than the first Km value measured after the end of hypoxia, indicating that hypoxia induced a compensatory change in the metabolic state of the tissue. Km increased immediately after both 5- and 10-min hypoxic insults and returned to normal after recovery for each case. It seems that during and immediately after short periods of hypoxia, Km increases from near zero but returns to normal values within a few minutes.

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