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Date: Wed, 14 Feb 1996 21:11:51 -0800
From: atikkan@ix*.ne*.co* (EE Atikkan )
Subject: Re: PO2 and bones
To: Robert Wolov <wolov@hi*.co*>
Cc: techdiver@terra.net
You wrote: 
>
>>Has anyone seen any updates on the theory that Osteonecrosis is 
caused
>>by elevated PO2s?
>
>Are you sure that's elevated PO2? I've not heard that theory, but as a 

>bone pathologist new to diving, needless to say I've a personal 
interest 
>in the topic.
>
>I'm at the Armed Forces Institute of Pathology and we've done some 
work 
>in this area. Our theory goes that the osteonecrosis (bone death) that 

>occures in dysbaric conditions 
>(doc-speak for the bends) is the result of more then just N2 bubbles 
>embolizing in the small blood vessels. Animal studies seem to show 
that 
>there is a 5-fold greater solubility of nitrogen in fat cells with a 
>swelling of the fatty tissue at the cellular level. (more reason to 
stay 
>in shape and not get overweight!)


Interesting point.  Has this work been published? Citation?
Thanks
>
>In soft tissue that's not such a problem, but the marrow fat in all 
our 
>bones (especially in such areas as the hips, knees and 
shoulders...where 
>coincidently you get most cases of osteonecrosis) is encased in a 
shell 
>of unyielding bone. As the fat cells swell, the pressure in the marrow 

>compartment goes up and decreases the already low blood flow to these 
>areas. We figure that the nitrogen transport out of the fatty tissue 
in 
>these areas is only about half of that in other tissues. Throw in low 
>oxygen partial pressures on top of sluggish blood flow and you 
>essentially strangle the bone. 

It was my understanding that dysbaric osteonecrosis was not a marrow 
problem as much a a natrix problem.  That appears easier to explain a 
hip collapse, the classical dysbaric osteonecrosis in commercial divers 
as opposed to a marrow effect.
>
>So it may be that there is a two-fold hit on "rapid" decoms. There is 
the 
>formation of bubbles (the classic theory) that is supported by the 
>observation of microscopic damage to the lining of small blood vessels 
as 
>well as doppler sound-wave detection of bubbles as well as the 
swelling 
>of fat cells in bone marrow, raising the internal pressures and 
reducing 
>the blood flow and supply to bone.

Again, citation?  Are we talking about ascents from saturation 
exposures or non saturation exposures.  As the question of bubbles 
coalescing is an issue.  Also how do they detect (via Doppler) bubbles 
in small blood vessels?  What is psotulated mech from blood vessel 
swelling?  Is this a gas phase separation of dissolved N2?  Appears 
relaatively unlikely unless the subject is saturated.
>
>What I need to do is start to "bone up" (sorry) on the various "tissue 

>profiles" 
Dive computers do not use tissue profiles.  The USN Tables, the 
Buhlmann Tables, the PADI Tables as well as computers that employ 
neoHaldenin models utilize 'compartments' & all emphasize that they do 
not correlate with any tissue or organ.  They are an abstraction, that 
sort of digitilizes the body - making it mathematically tractable.

that are used in the commercial dive computers so I get a 

[balance clipped]

Esat Atikkan
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