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on 6/26/00 12:09 AM, Randy F. Milak at milak@di*.zz*.co* wrote:
> Mr. Markwell was looking for definitive proof of this drug to
> be a panacea of DCS. It clearly is not.
To be clear, if I understand this statement correctly, I was not looking for
proof of aspirin as a panacea to prevent DCS. There is no such thing. The
word "panacea" implies a broad cure, I don't think anyone has suggested that
aspirin is such a thing or ever could be. IF aspirin works at all to prevent
DCS, it works as part of an overall regimen that includes conditioning,
hydration, being drug-free (including nicotine), and all the other steps
technical divers take to deco-dive successfully.
What I was looking for was good science that it works specifically as a step
towards preventing DCS. To date I have yet to see such proof. The only study
I've read that implies that it might, appears to say that it is inconclusive
and that the effect of platelet aggregation as part of the mechanism that
leads to DCS is not even fully understood and therefore can't even be
definitively said to be one of the primary steps in the unfolding of DCS in
the human body.
I'm sure there is more literature and it may contradict my statements here,
but I haven't seen them. I'd like to see them.
What I'm objecting to is the clear implication by, apparently all parties,
that aspirin works in this area as an effective element in the steps taken
to prevent DCS. It's become like herb industry. Claims made, but no proof.
I've yet to see anything other than intelligent extrapolations citing what
aspirin does in the human body and that along with what we believe about DCS
leads one to conclude that therefore it must work as suggested. Intelligent
"if-then" extrapolations may be well thought out and even inspired, but they
can also be 100% wrong.
JoeL
That study is quoted again here:
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
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