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> >As I learn more and more about CNS O2 toxicity, I become less and less
> >convinced that accumpated "dose" (i.e., prior exposure) has much
> influence
> >on probability of convulsion.
>
> Are you speaking strictly of prior, low PO2 (<1.5) exposure?

Yes. I was referring specifically to the "O2 clock" concept, which
supposedly chips away at your ability to tolerate high PO2, even while you
are breathing <1.5 PO2.

> If not, I
> would disagree - Have you read that article by Johnny Brian?
> Although, I'm
> sure you are otherwise you basically get into a magic P02 that instantly
> causes seizure, and that's definately not the case.

There is no "magic PO2", but there may be a "magic threshold set", which
would be a set of threshold conditions (only one of which is inspired PO2;
other may include CO2 and any number of other physiological paramters)
which, within the chaotic context of our physiology, trigger a seizure.

I am sure there is some time component to O2-induced seizure.  The question
is, is it mostly a short-term (few minutes) effect (e.g., on a scale of time
required for the high dissolved O2 in the blood to prefuse to the critical
tissues), or does it also consiste of a long-term (many minutes to hours)
effect (e.g., some sort of biomolecule becoming oxidized over time, and a
seizure is triggered when the rate of said biomolecule repair can't keep up
with said biomolecule destruction).

I'm not familiar with the article you mentioned (reference?), but I've yet
to see and real evidence supporting the long-term effect.  From what I've
read, absolute inspired PO2 is likely more of a factor (e.g., instantaneous
risk) than cumulative historical O2 exposure (e.g., increasing cumulative
risk).

Aloha,
Rich

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