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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? Yep! My chairman, Donald Sweet wrote the chapter on osteonecrosis with all the citations in the 5th volume of Resnick & Niwayama's Diagnosis of Bone and Joint Disorders (Saunders) Sorry not to cite it...figured that no one would want to hear all that medicalese. > >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. It's actually both. It's tough to isolate the cancellous bone circulation (I'm assuming that's what you mean by matrix) from the marrow microcirculation. The actual physical collapse of the joint's articular surface is actually the result of the body's healing process. As the body attempts to resorb the dead bone cells and replace with new replicating osteocytes you reach a point where you've removed more dead structural host bone and not laid down enough new bone...like trying to swap out the bricks in a wall while it's still standing...you reach a point where the wall collapses. We see the same thing in such conditions as Perthes' Disease where the femoral epiphysis slips and blitzes the circulation. Some observers think that the osteonecrosis seen with steroid use might be related to the same mechanism, swelling of the marrow fat cells with increase in intramedullary pressure. To the best of my knowledge that was in animal studies between AFIP and Walter Reed. I think it was published but I don't have a citation off the top of my head. Can't understand why humans won't let us take them to the OR just to biopsy pieces of themselves to see what's going on! > >Again, citation? Same as above...Resnick & Niwayama >Are we talking about ascents from saturation >exposures or non saturation exposures. I'm really not sure. I know that the original data cited in the text was based on tunnel workers not divers. Not sure how these two groups correlate. There must be at least some differences at some level. I defer to the real hyperbaric docs on this one. >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. The micro doppler issue is a research question. I've no direct hands on experience with the technique. However, it never ceases to amaze me how the resolution of these instruments has increased over the last few years. The blood vessel swelling is somewhat limited to the endothelial inner lining. It seems that this endothelial swelling is a reactive phenomenon seen pretty much in any blood vessel injury (thermal, atherosclerotic emboli, infection). I'm not sure and I wouldn't even begin to speculate whether this is the result of direct irritation by frank bubbles or just the result of gas exchange across the cell membrane or both. It's easy to forget that the dissolved gas doesn't just leap from lung alveoli to blood and back again. It crosses a number of cell membranes in the process and the response of those cells may vary depending on cell type, type of gas, degree of saturationl, etc. I have no idea to what degree these factors have been studied. Keep in mind that I'm a bone pathologist not a gas physiologist. My other hat is that of a Navy flight surgeon. Still going the wrong way since we are forever decompressing our patient's where divers are getting compressed...and to a much greater degree. A diver only has to go 33 feet to double his pressure while an aviator has to ascend to tens of thousands of feet (even then they pressuraize the cockpit generally). Hey, I'm still trying to learn to control my buoyancy without looking like I'm all arms and legs! ;-) >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. > I stand corrected. I got sloppy with my terminology. I've heard divers (my instructor for one) refer to the "tissue profiles" in discussing computers and didn't want to confuse the issue by trying to correct everyone's lingo. (not to mention irritate the h*ll out of folks...though I already may have done that!) I'm in absolute agreement with you over the complexities of the body as a multiphase system. If only we could reduce the physiology to a nice simple equation! To paraphrase Lazarus Long...much of nature can be reduced to simple, easily comprehended, *AND INCORRECT* explainations. I wish the body's gas physiology was one of them...then maybe I could understand it! Total aside: Are you the "Atikkan" from NIH that our Major Anderson keeps refering to? If so, then I was suppose to look you up in order to get involved with the local diving activities of the "Germantown Boys & Girls". I'll just be doing my basic and advanced open water dives this weekend (3 days worth!) so I figured you wouldn't want to bother with someone like me until I had my C-card and was a "real" diver (confined pool dives don't count!) To the other divers on this list: My apologies for the long wind...I'll shut up now and go back to my corner! Robb Wolov
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