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Date: Mon, 20 Jul 1998 15:04:17 -0400
From: Bill Mee <wwm@sa*.ne*>
To: Jack Kreska-FJK003 <Jack_Kreska-FJK003@em*.mo*.co*>
CC: john.r.strohm@bi*.co*, techdiver@aquanaut.com
Subject: Re: The Beat Goes On: Hyperoxic Oxygen
Hyperoxic oxygen is perhaps the single most dangerous factor in
technical diving. There are many reasons for not exposing oneself to
high ppo2s not the least of which are seizures and death. To recommend
the breathing of high o2 mixtures is both frivolous and reckless
particularly  when the consequences of high oxygen exposure are
considered. 

We know a lot more now about the consequences of high ppn2s and high
ppo2. The WKPP drastically modified it's practices with regard to oxygen
exposure following the collective experience of many lengthy
decompressions and the varying levels of pulmonary distress.  Once you
are aware of the seriousness of what hyperbaric oxygen does you may wish
to rethink how much exposure you care to subject yourself to. 

The Hemoglobin oxygen buffering system is a remarkable evolutionary
adaptation which allows humans to exist at oxygen tensions substantially
lower than what we encounter at sea level.  Even with  alveolar oxygen 
levels at 100 mmHg ( .133 Ata Ppo2) the hemoglobin is 97% saturated.  
This system unfortunately is incapable of maintaining the normal 40 - 60
mm Hg capillary tissue tension when the alveolar po2 rises beyond 2 ata.
When this happens the level of dissolved o2 (non hemoglobin bound) in
the blood rises uncontrollably and with it the presence of oxygen free
radicals such as the superoxide and the peroxide free radical.  These
oxidizing free radicals swamp the enzyme systems for removing them and
have a serious destructive and possibly lethal effect on cells.

Ordinarily, the body's system of peroxidases, catalases and superoxide
dismutases
mops up these radicals. Almost any college text on biochemistry broadly
details the mechanism and kinetics of these reaction mechanisms. The
vitamin E family (tocopherol isomers) is known to play an important role
in this antioxidant management system. You will note that the alveolar
tissue component is exposed to the direct effects of high oxygen without
the benefit of the buffering system. This is probably why even moderate
exposures of o2 at 1 ata and slightly above  cause observable functional
deficits (Clark and Lambertsen 1971 and Clark 1988).

The first victim to go down, following the collapse of the
hemoglobin-oxygen buffering system, are the polyunsaturated fatty acids
that are fundamental components of cell membranes and connective tissue.
Many cellular enzymes, both free and membrane embedded are oxidized,
challenging many metabolic systems dependent on  these enzymes.
Neurological tissues are particularly vulnerable given the high lipid
content of axonal, soma and dendritic structures in nerve cells.  This
probably accounts for the extremely acute damaging effects of hyperoxia
on brain function such as seizures. Other complex neurological tissues
such as the eye and its components (retina) suffer quantifiable
deficits.

When you are honking on pure oxygen at 20ft and think that dropping down
to 30ft will give you better results I suggest you seriously think
again. Even worse don't even think about doing a working dive at 1.6 ata
ppo2.   For anyone who advocates diving at 1.8 ata ppo2 I say let them
have at it themselves validate Darwin's theories of natural selection.

Regards,

Bill Mee



Jack Kreska-FJK003 wrote:
> 
> Well, John,
> 
> Why don't you write a well-written response to Dive Training? People
> continue to talk about this stuff but the only thing we do is gripe
> among ourselves.
> 
> Jack
> 
> -----Original Message-----
> From: john.r.strohm@BI*.co* [mailto:john.r.strohm@BI*.co*]
> Sent: Monday, July 20, 1998 7:57 AM
> To: techdiver@aquanaut.com
> Cc: cavers@ca*.co*
> Subject: The Beat Goes On
> 
> "Dive Training" magazine, August 1998, p. 14.
> 
> Letter to the Editor from one Bret C. Gilliam, decrying the magazine's
> stance on ppO2(max).
> 
> "Dive Training" ran an article recently that, among other things,
> recommended a ppO2(max) of 1.4 ata.  Gilliam is saying that 1.6 ata
> ppO2(max) is perfectly OK, provided the NOAA time limits are also
> observed.
> 
> And the problem is that the world is going to read this, and say "This
> is
> one of the big guys and he must know what he is talking about".  And
> Gilliam's List will continue to grow.


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