Aspirin and Diving

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Interesting that the mortality was so heavily impacted, but neuro symptoms were not. It makes you wonder if the mortality was due to pulmonary dysfunction (chokes) which is fairly severe DCS.
It isn't clear in the paper but apparently some animals died during the experiment so it looks like the Neuro DCS were those who showed symptoms but didn't die. So in the control group of 49, 35 died and 12 of the others showed neuro DCS which really is 12/14.
Bill
 
Do you know the references the authors cite to support these claims? Is their data primarily from animal models? I don't subscribe to this journal or I'd look it up myself...

E.g.:

"J Appl Physiol. 2009 Dec;107(6):1825-9. Epub 2009 Oct 22.

Bubble-induced platelet aggregation in a rat model of decompression sickness.
Pontier JM, Vallée N, Bourdon L.

1Medicine Department, French Navy Diving School, Toulon Army, France.
jm.pontier@free.fr

Abstract
Previous studies have highlighted that bubble-induced platelet aggregation is a predictor index of decompression sickness (DCS) severity in animals and bubble formation after a single air dive in humans. The present study attempted to investigate plasmatic indexes of the coagulation system and platelet activation in our rat model of DCS. Male Sprague-Dawley rats were assigned to one experimental group with a hyperbaric exposure and one control group maintained at atmospheric pressure. Rats were compressed to 1,000 kPa (90 m saltwater) for 45 min while breathing air. The onset of death time and DCS symptoms were recorded during a 30-min observed period after rats had surfaced. Plasmatic indexes were platelet factor 4 (PF4) for platelet activation, soluble glycoprotein V (sGPV) for thrombin generation, and thrombin-antithrombin complexes for the coagulation system. Blood samples for a platelet count and markers were taken 3 wk before the experimental protocol and within the 30 min after rats had surfaced. We confirmed a correlation between the percent fall in platelet count and DCS severity. Plasmatic levels of sGPV and PF4 were significantly increased after the hyperbaric exposure, with no change in the control group. The present study confirms platelet consumption as a potential index for evaluating decompression stress and DCS severity. The results point to the participation of thrombin generation in the coagulation cascade and platelet activation in bubble-induced platelet aggregation. In our animal model of DCS, the results cannot prejudge the mechanisms of platelet activation between bubble-induced vessel wall injury and bubble-blood component interactions."

Regards,

Doc
 
E.g.:

"J Appl Physiol. 2009 Dec;107(6):1825-9. Epub 2009 Oct 22.

Bubble-induced platelet aggregation in a rat model of decompression sickness.
Pontier JM, Vallée N, Bourdon L.

1Medicine Department, French Navy Diving School, Toulon Army, France.
jm.pontier@free.fr

Abstract
Previous studies have highlighted that bubble-induced platelet aggregation is a predictor index of decompression sickness (DCS) severity in animals and bubble formation after a single air dive in humans. The present study attempted to investigate plasmatic indexes of the coagulation system and platelet activation in our rat model of DCS. Male Sprague-Dawley rats were assigned to one experimental group with a hyperbaric exposure and one control group maintained at atmospheric pressure. Rats were compressed to 1,000 kPa (90 m saltwater) for 45 min while breathing air. The onset of death time and DCS symptoms were recorded during a 30-min observed period after rats had surfaced. Plasmatic indexes were platelet factor 4 (PF4) for platelet activation, soluble glycoprotein V (sGPV) for thrombin generation, and thrombin-antithrombin complexes for the coagulation system. Blood samples for a platelet count and markers were taken 3 wk before the experimental protocol and within the 30 min after rats had surfaced. We confirmed a correlation between the percent fall in platelet count and DCS severity. Plasmatic levels of sGPV and PF4 were significantly increased after the hyperbaric exposure, with no change in the control group. The present study confirms platelet consumption as a potential index for evaluating decompression stress and DCS severity. The results point to the participation of thrombin generation in the coagulation cascade and platelet activation in bubble-induced platelet aggregation. In our animal model of DCS, the results cannot prejudge the mechanisms of platelet activation between bubble-induced vessel wall injury and bubble-blood component interactions."

Regards,

Doc

Bubble-induced platelet aggregation in a rat model... [J Appl Physiol. 2009] - PubMed result
 
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