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on 6/15/00 7:56 PM, Geoff Kelafant at kelafant@we*.co* wrote:
> Medications per se are not necessarily disqualifying but often the condition
> they are prescribed for may be a contraindication to a number of activities,
> scuba diving included.
Geoff,
My question is specifically related to prophylactic use of ibuprofen and
aspirin to prevent or help to prevent DCS. Is it effective? Where can I see
research on this specific question?
Most of what I've read indicates that aspirin MAY have some use in this
area, but one study (below) seemed to indicate that it doesn't seem to do
what it ought to do and its use may be very limited and that other drugs
(VK744) are more useful but carry with them more side-effects. It finally
draws no absolute conclusions.
That study I include below:
SNIP>>>
Hematology and blood chemistry in saturation diving: I. Antiplatelet
drugs, aspirin, and VK744.
Philp RB, Freeman D, Francey I, Bishop B
Blood chemistry and cellular parameters were studied before, during, and
after saturation (2.4 ATA) dives in the HYDRO-LAB habitat on two separate
occasions. In both, platelet count fell greater than 20% 12-24 hours after
surfacing and moderate (5%) reductions in hemoglobin, red-cell count, and
packed-cell volume were observed. Plasma cholesterol and triglyceride levels
were depressed postdive as were most plasma enzymes (GOT, GPT, CPK, LDH,
ALP). The latter changes were very slight. In the first study, the
incidental ingestion of aspirin by some divers did not prevent the loss of
platelets even though the platelet-release reaction in response to ADP was
inhibited. In the second study the platelet-suppressive drug VK744 was
administered, on a double-blind randomized basis, to six divers, six others
taking a placebo capsule. Dosage of VK744 was 300 mg TID for 2 days before,
5 days during, 3 days after saturation dive. The drug inhibited the postdive
loss of circulatory platelets and in fact the treated group showed a rebound
in platelet count above control values, 48-72 hours postdive.
Megathrombocyte counts indicated the production of new platelets in both
groups at this point. The treated group also showed a marked and significant
reduction in plasma cholesterol and triglycerides, suggesting an
antilipidemic effect of the drug. Theses results confirm previous
observations and indicate that postdecompression loss of platelets may be
related to sequestering of reactive platelets, possibly by microbubbles, and
that the phenomenon can be inhibited by some antiplatelet drugs.
<<<SNIP
I'm not trying to rain on anyone's parade here, I'm just trying to find out
what is actually KNOWN and not what is BELIEVED.
Later,
JoeL
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