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From: trey@ne*.co* (Trey)
To: "Esat Atikkan" <atikkan@ya*.co*>, <techdiver@aquanaut.com>
Subject: Re: General DCS Information
Date: Sun, 18 Jun 2000 06:04:17 -0400
Esat, we just use them to keep the body's immune response to bubbles and
damage muted somewhat. I am not even sure if they work at all as a
prophylaxis, since I get no difference with or without them on identical
dives. I use piroxicam 2 X 20 mg as that one lasts 24 hours whereas the
ibuprofen and others seem to get metabolized by the liver too quickly to
last as long as the dives that I am doing.

Otherwise if  we exercise too much at depth we get an effect like a huge
workout on the joints, and it seems to keep that under control somewhat, but
the damage is still being done, it is just the inflammation that is not as
severe with the drugs, or so it seems.

That is the simple version, maybe if you have time you could do one on the
immune response mechanisms and I'll put it on our web site - don't worry
about the creative phonetics - we can all read "Esat".

From: Esat Atikkan <atikkan@ya*.co*>
To: techdiver@aquanaut.com <techdiver@aquanaut.com>
Date: Saturday, June 17, 2000 11:53 PM
Subject: Re: General DCS Information


>
>
>Finding an adequate model to deal w/ DCS or DCI is
>frustrating to say teh least.
>Indeed some studies have shown blood chem changes,
>though the significance remained meagre.
>Same goes fro the immunological changes that Ward et
>al pushed for a # of year.
>
>The issue is a model that depends on bubbles being the
>etilogical agent.  Yet no one has been able to show a
>causal relationship b/ bubbles & DCS.  A dose-response
>relationship (applying the Koch principle) has been
>even more elusive.
>
>So it has been empirical - the bubble notion, coupled
>w/ HBO works, so lets keep 2 it.
>
>As for platelet aggregation & the use of
>anti-coagulants.  Best I recall the jury is out.
>Theory does support the nifty picture of a N2 bubble
>w/ the hydrophobic ends of fatty A+ sticking in, their
>hyfrophilic ends out, representing foci for platelet
>aggregation - microthrombi @ work.  But no one has
>conclusively shown them - I am willing to B corrected
>on this if there is evidence.  Then again how does
>that extrapolate to DCS of He diving.
>
>So the issue remains - what does aspirin (salicyl
>acetate) do?  Well aspirin is an analgesic.  It does
>help w/ pain.  DCS produces pain - hmmm!  Hence the
>advise against aspirin in the context of diving - a
>pain killer takes away the primary diagnostic tool.
>
>Francis has held that DCS is really a very diffuse
>disease (Disseminated Vascular Disease as he calls
>it). This is a tidy definition because it covers all
>aspects of the etiology w/o committing itself to any
>specific measurable parameter - sort of the reason why
>an objective test for DCS has been so elusive.
>
>A threshold concept that models a # of the rheological
>changes may have to B invoked as CPK changes, Ig
>changes, platelet aggregation have all been reported -
>yet none has been significant enough to provide the
>diagnostic tool.
>
>U dives & U takes your chances - bubbles or no
>bubbles, platelet aggregation or no platelet
>aggregation, 5a up or down.  Thus in thinking
>prophylaxis one has to 1st question what is really
>known about the mechanism/pathway by wh/ the
>protective agent could plausibly act on the etiology,
>where that also remains cloudy.
>
>Hey mayB we thnk science too much.
>
>Safe bubbles (whatever they R)
>Esat Atikkan
>
>
>
>
>> I'm not trying to rain on anyone's parade here, I'm
>> just trying to find out
>> what is actually KNOWN and not what is BELIEVED.
>>
>> Later,
>>
>> JoeL
>>
>> --
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>
>
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