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> I have a question about this!! Say it would be possible to offset O2 > toxicity symptoms. You can only metabolize so much oxygen, and after > that point is reached the oxygen would then be dissolved into ones system > unused. Provided no toxicity problems occured, it would then be possible > to become bent on oxygen. If this is possible, I would guess that the > decompress schedule would be lighter due to not only the offgassing of O2, > but the metabolizing of O2. It could also be guessed the the greater the > workload the less the decompression schedule. My question is then would > it be possible to dissolve this much O2 into the body to cause > decompression concerns? > Then, with the recent debate of O2 narcosis, would it be worse > then N2 narcosis, and therefore feasible to do this? Tony brings up a couple of interesting points here. Oxygen is not taken into account for decompression calculations mostly because it only becomes significant (from a decompression standpoint) at PO2s way in the CNS toxic range. However, in the event that O2 toxicity can in some way be pharmacologically supressed (not bloody likely, but lets entertain the notion for the sake of argument), then oxygen may, indeed, become a significant factor in decompression calculations. HOWEVER, as Tony points out, O2 is constantly being metabolized, so an O2 bubble should resolve much faster than a bubble composed primarily of N2. But even if it doesn't resolve faster (say, for example, dissolved PO2 is maintained very high in the blood), would an O2 bubble be as problematic as an N2 or He bubble? If the main damage caused by DCS bubbles is tissue-level hypoxia from obstructed capillaries, then would the damage be minimal or entirely absent if the dissolved PO2 is kept so "freakin'" high as it would in such a case? If hypoxia were happening on the downstram side of the bubble blockage, then the O2 gradiant on that side of the bubble blockage would cause rapid "offgassing" from the bubble to the blood, would it not? (I realize this is a function of the rate at which O2 diffuses through blood). On the other hand, if the circulatory blockage is not caused by the bubble per se, but rather by platlet aggregation around the bubble, then perhaps localized tissue hypoxia would occur anyway. Does anyone have any thoughts on this? As for narcosis: as someone who has breathed pure O2 at a simulated (chamber) depth of 220 feet, I can report that, as far as I could tell, the narcosis severity was approximately equal to what I would have experienced at the same depth breathing air. Aloha, Rich
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