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Several people have asked me privately about the effect
of high partial pressures of nitogen on the circulatory system. I
will explain the basics, but if we could get Ali Lawrie to take over
from these, or one of the other medical types, it would raise the
level of the discussion, and preclude the "qualified to discuss"
agrument. I know it because any undergraduate course in hemodynamics
covers it, and this is the type of information I seek before I put
my
ass on the line.
The red blood celss are biconcave disks which deform and
allign themselves axially as they move through capilalaries whose
diameter is smaller that that of the RBC. This microcirculatory
effect
is very critical to the oxygenation process of tissues. The intimate
contact is what provides the better gas transfer. When these cells
do not deform, but remain rigid, they trigger the stretch receptors
in the vessels (which is somewhat nomall) except when there is no
good reason for it in the first place. Normally this function would
be reserved
for the response to microinjury sites or immune system responses.
When these cells become rigid due to the elevated
nitrogen
tension , microcirculatory insult results, followed by all of the
autoimune
resonses thereto, which then will set up for DCS. This is the level
where the most insideos DCS can occur, as in the brain.
As I have already been flamed on this by some real
geniouses,
I will say no more other than to tell you to go to the library, or
persude
one of the medical types on here to finish this. I will say that at
least
I have done my homework, have the training agencies?
Since I am trying to provide good information here, I do
not
expect to be attacked on this one. Keep me out of this discussion
from here on . - George
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