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>Not to take either side here (yet) but . . . on the other side of the coin >we have divers who have no problems with extremely high O2 exposures one day >and take a hit on moderate exposure another day. I seem to remember >reports >of rare occasions of people toxing in hospitals on 1 ata - CNS. There are, as you know, exceptions for everything... As I said, in the context of deco in ocean rough water, I do not believe that using the argument of transient raised PO2 to justify using "stroke" deco mix is justifiable. > I find your reference to "Oxygen Scavengers" interesting. I cannot >picture a mammal such as ourselves evolving a defense mechanism against >something so unlikely to encounter in our natural environment as high O2. >Chances are that the binding of O2 is not the drive behind the evolution of >these "scavenger" molecules, rather that they normally facilitate an entirely >different function and this is a coincidental event - probably detrimental to >the blood and systemic chemistry. > Also there is a big difference between binding to a free radical (singlet >O2) and capturing a diatomic gas molecule. Which are you saying these >scavengers do? Obviously, they will deal with free radicals. The presence of these oxygen scavengers can be explained easily if we remember how our immune system works. Immune effector cells often rely on oxydating damage to kill/destroy antigens. Other ways to deal with oxygen involve enzymes (peroxydases), hemoglobin and hemoglobin-like molecules (which, as you know, deal with O2). Vitamins present in the system can also act as oxygen scavengers (these are often referred to as anti-oxydant). >If these "scavengers" are in place and capture diatomic O2 how does O2 get >past them to enter the cells after dissociating from Hb and how long would >the >processes of normal respiration take to deplete these defense molecules? If >they only bind to singlet O2 what process breaks down the O2 molecule to make >the radical available. I think that both diatomic oxygen and free radicals are involved in the toxicity. Narcoric effects on the CNS are probably due to O2. Acute CNS toxicity has probably something to do with both free radicals and O2. Pulmonary toxicity is probably due mostly to free radicals. Interestingly, chronic oxidative damage is one of many theory currently regarded to explain aging. > How do you figure that brief exposures will be benign considering the rate >at which chemical reactions occur in the blood if these toxicity problems >stem >from such events as the depletion or overwhelming of defensive chemistry ? Brief increased gas density will probably not have an immediate effect on physiologic parameters. For the blood to become at equilibrium with the outside gas pressure, time is necessary. In the context of deco in rough water, I doubt that enough time will be available between waves to allow the blood to reach that equilibrium with the transiently increased PO2 of the inspired gas. Other variables such as frequency of breathing and lung volume while the PO2 gets increased by the passing of the wave are to be considered. If you happen to have expired while that wave was passing, you have a little volume of air having less than 100% O2 remaining in your lungs. Blood PO2 will thus not reach the theoretical dangerous PO2. Taking all this into consideration, keeping all this into the context of ocean deco, I still believe that transient increase in PO2 while decompressing with 100% oxygen is not likely to be harmful. If you add to that the fact that you are actually moving with the column of water, the risk become even less since the PO2 gets less affected. > Lest this start another thread on O2 radicals note that there is so much >plasma bound O2 available to the system on air at one atmosphere that the >addition of a few zillion more molecules, as when diving, would probably kill >us in short order by total destruction of the blood chemistry if it >contributed to the production of more radicals. O2 and free oxygen radicals are probably on a state of dynamic equilibrium. O2 bound to Hb is probably not too involved in that equilibrium since it is dealt with but free (or plasma) O2 must be involved. >All this extra O2 just goes along for the ride in the blood as a diatomic >molecule without being broken into dangerous radicals. Though the >mechanisms >of toxicity problems is not well understood I think it is safe to assume that >both CNS & OTU toxicity result from localized interactions with the diatomic >form, not from widely dispersed radicals in the blood or tissues. You may be right. But free radicals may contribute (and this is only an hypothesis) to the diatomic toxicity by causing physiologic changes (alteration of blood flow, shifts in the Hb-O2 dissociation curve and other things alike) that may affect the way diatomic oxygen is handled by the system. But this, of course, is a little "hors contexte" regarding the initial message about using pure oxygen as a deco gas for ocean dives. We can only speculate now since, as you mentionned, most of the mechanisms involved in oxygen toxicity are not well understood. What an interesting subject isn't it? Etienne -- Send mail for the `techdiver' mailing list to `techdiver@aquanaut.com'. Send subscribe/unsubscribe requests to `techdiver-request@aquanaut.com'.
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