pufferfish
Contributor
Hi Dr. Deco,
Boy that last sentence seems to be an understatement after reading about the shuttle probe report and listening to an interview with Prof. Vaughan from Boston U. last night. Forty percent cuts to staff and budgets certainly doesn't leave a lot of $$ for DCS research I imagine. She also stated that management felt the risk of such a catastrophic 'accident' was 1/100,000 but that if you asked the engineers on the ground they would estimate 1/25. I am sure the poor astronauts were not aware of those numbers. Sounds like management needs a big shakeup with a refocusing on safety and not on cost cutting and scheduling efficiency.
I had a quick look to see if I could find any further references to bubbles initiating the inflammatory cascade in DCS and found this one from the Swedish military. Very interesting study but what these guys are missing (and this is also still the case in the ID literature although changing) are the levels of cortisol produced during hyperbaric stress. As the last sentence suggests there is a balancing act between the pro and anti-inflammatory cytokines but that little 'dance' is under the control of the much larger HPA axis. These young healthy military recruits would have very robust HPA systems which could produce sufficient levels of cortisol to dampen any pro-inflammatory activation that might ensue from a bubble load within a NDL dive. An interesting study would be to look at the HPA axis reserve in a group of recreational divers from across all age groups and then take them down to the maximum NDL and measure these cytokine balances. My hunch is those that had sub-optimal HPA axis challenge tests prior to diving would be the first to show evidence of pro-inflammatory cytokine activity and the most likely to experience DCS. Take this same group with evidence of adrenal insufficiency (poor HPA axis reserve) and infect them with SARS or give them a bypass operation and they will also have much higher morbidity and mortality. Whether bubbles, infection, or surgery these are all 'stressors' to the organism which are handled by the same common pathways.
Hyperbaric exposure and inflammation
If you are getting tired of reading that new Bennett and Elliot book
, may I suggest an excellent source for many of these ideas and although often discussed in infectious disease terms one only has to substitute bubbles as the initiating pathogen. Yes the cytokine signatures are different for different pathogens and tissue damage depends on where the pro-inflammatory cytokines are released, but the mechanisms to control these reactions are all much the same once the cascade has begun. In part V, section 19 the work by Christine Biron is most fascinating and she has been of late branching out and looking at how the environment ( how what we as individuals do in our daily lives) can influence the HPA axis and resultant disease expression. In other words lack of fitness, obesity, lack of sleep, and poor diet all impact to lower one's HPA reserve and hence cortisol responsiveness which predisposes us to all sorts of morbidities and sometimes mortality when disease hits. This is likely the biological basis for our 'constitution' and why we see forty year old patients dying from SARS amongst the older seventy year old folks. A person's chronological age may be forty, but the physiological age of their HPA axis reserve might be seventy years likely reflecting years of HPA axis abuse, but what constitues that abuse is a whole other story 
Coping with the environment: Neural and Endocrine Mechanisms
Anyhow lots of interesting work to be done but like the ID people who have had to step out of their viral and bacterial 'boxes' and learn about the HPA axis in disease, I suspect most barophysiologists will have to as well in order to truly understand DCS.
Interesting what one can find on the Net regarding DCS.
The Butterfly Effect
Thanks again for your responses and I hope things improve (read more $$$ for DCS research) at NASA.
Cheers,
Pufferfish
