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On Wed, 19 Jun 1996, David Doolette wrote: > Making the reasonable assumption that CNS O2 toxicity is a manifestation of > toxic build up of reactive oxygen species, one would expect that the build > up of ROS to some "toxic threshold" would follow an exponential curve of > some sort since (forgive my elementary grasp of mathematics): > dC.ros/dt = K1*C.O2 - K2*C.ros > where C.ros is the concentration of reactive oxygen species in the tissue, > C.O2 is the concentration of oxygen in the tissue, K1 is a rate constant for > the formation of ROS and K2 is for the destruction of ROS. > Since individuals would have different rate constants the accumulation of > ROS would vary, and since individulas would have different "toxic > thresholds" the incidence of convulsion against time would be distributed > (let us say) approximately normally (this actually isn't supported by animal > experiments). The integral of such normal curves would explain the > approximately sigmoid survival curves illustrated in the NNMRI paper. > > I can't imagine that gas transfer at the tissue level has anything to do > with CNS O2 toxicity. Presumably, O2 toxicity is dependent on arterial PO2 (PaO2) or at least the change in PaO2. From patients on ventilators, we know that hyperbaric O2 and resultant pulmonary O2 toxicity actually lowers the PaO2 - perhaps this works as come kind of protective mechanism. I suspect that even in the short term there are local pulmonary changes in gas transfer. - PH > Looking at venous O2 concentrations, which presumably > reflect tissue concentrations if you believe in flow limited gas kinetics > (which are a reasonable approximation), oxygen does not behave like an inert > gas and accumulate in tissues with inspired PO2 less than 2 bar. As an > off-the-cuff thought, perhaps this explains the 2 bar asymptote for oxygen > toxicity against time seen in tissues other than the lungs (which see the > inspired PO2). > > regards, > > David Doolette > ddoolett@me*.ad*.ed*.au*
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