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Loading the blood/serum compartment with various solutes >could<
change the solubility of N2, but it would probably have to be a LOT
of the substance. Since the blood is already pretty loaded with pro-
tiens, polypeptides, fatty acids, what have you, I'm not sure if it
would be very easy to radically alter the solubility of N2, or even if
it would be desirable to do so; anyway, you'd only be altering one or
two of the many compartments that decompression models consider. Which
way would be advantageous?

My (not complete, I'll freely admit) understanding of DCS is that you
get "hit" when bubbles reach a certain size, but that this size is
smaller than the size that would be damaging, if the bubbles were only
nice, clean naked bubbles. The body, however, reacts to the bubbles;
protiens (and possibly other bio-molecules?) glom onto the bubbles,
making them bigger, more irregular in shape, and stickier. I then imagine
that the buggers grow like a snowball rolling downhill in a cartoon,
attracting more and more bio-molecules onto themselves. It's these large,
gooey objects that do the actual clogging, etc. (as an aside, I imagine
that it is *possible* to so saturate your body with N2, and surface so
rapidly, that you actually do fizz your blood with macroscopic bubbles,
but I doubt you'd even get back to the boat. Maybe any SAT divers listening
in can enlighten us as to this gruesome scenario?).
I don't think that this is how sport divers get bent.
 Point is, altering this secondary immune (immune-like?) response might
be a more fruitful way to proceed, not that I have any idea as to how
to do so, other than the oft-discussed and not new theory that frequent
diving can deplete your supply of the specific protiens, antibodies,
etc hat are involved, thus affording some defree of protection.

Dave (defree?) Ventre
Quincy, MA

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