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Date: Fri, 16 Jun 2000 08:36:48 -0700 (PDT)
From: Esat Atikkan <atikkan@ya*.co*>
Subject: Re: General DCS Information
To: techdiver@aquanaut.com


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
> 
> --
> Send mail for the `techdiver' mailing list to
> `techdiver@aquanaut.com'.
> Send subscribe/unsubscribe requests to
`techdiver-request@aquanaut.com'.


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