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	The discussion of cold vs hot narcosis has been interesting to
watch.  One comment on the following;

> 
> The "Cold Narc" effects do seem to be related to higher than normal CO2.
> This could be related to the inability of the blood to xfer O2 and CO2 to/from
> the lungs and tissues properly due to raised levels of gases in all three.
> When the pressure in the lungs increases it is xfered to the blood and from
> the blood to the tissues.  Reversing this action with CO2 on the return trip.
>  As the level in the tissues increases eventually the level in the blood
> reaches the point at which it can no longer effectively absorb/bond with
> more gases.  Therefore on the return trip it fails to bond with enough CO2.
> 
> (Please be kind, this is not based on anything other than the first thing
> that came to my wandering mind)
> 
> Have Fun,
> 
> Scooter

	CO2 is a 'special' gas in my book because its transport in the
body is unusual and not what was stated above.  Haemoglobin does not
bind CO2, only O2 and CO.  If it binds CO, it does not readily release
it, which is why one dies from CO inhalation.

	O2 as we all know is primarily transported by hemoglobin in
the red blood cells (at one atmospere!  At pressure, I don't know what
the loading levels are, but this is known.).  In the tissues, CO2 is
produced by the metabolism of O2.  Unlike N2 or Ar, or most other
gases, CO2 is NOT transported in the blood as a neutrally dissolved
gas.  CO2 is dissolved in the blood liquid as H2CO3 (Carbonic acid),
which changes the pH and helps release the O2 from the haemaglobin,
along with Di-Phospho-Glycrerol(DPG) in the tissues.  During the
transport of the blood from the tissue to the lungs and back, only a
small percentage of the total CO2 present in the blood (at 1 atm!) is
released in the lungs.  When the H2CO3 passes through your lungs, the
carbonic acid is converted to CO2 by an enzyme (carbonic anhydrase) at
rapid speeds in your lungs, thus causing the CO2 to outgas in a 'safe'
area.  I know that model calculations have been done to model the
effect of higher CO2 levels on the action of the enzyme, but since the
enzyme is limited by the rate of diffusion of CO2 INTO the enzyme, it
should (that's an opinion folks) work at at least the same RATE as on
the surface.  However, because the partial pressures in the lungs are
higher at depth, plasma loading of carbonic acid will increase.  The
(probable) shift in pH and the presence of more CO2 may well cause the
effects mentioned by Rich Pyle and others.

	Safe diving,

			Peter David

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