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The following text taken from internet is quite illuminating.
It explains how Aspirin and related drugs affect blood chemistry and the
possible effects on divers.
Subject:
DIVING and ASPIRIN USE
As
for ibuprofen while diving, 800 mg every 4 hours or even as a
pre-dive
ritual seems excessive, as you probably only need one 200 mg
tablet
in a 24-hour period. God almighty you guys must bleed like
hell
if you ever cut yourself (ibuprofen prolongs bleeding time just
like
aspirin, not to mention the effects it has on your stomach).
It's next
to
impossible to give any hard line "best effect dose" which attains the
best
of ibuprofins benefits with the least amount of side affects. I
would
submit that it's part science, and part 'art' on behalf of the
diver.
High doses are definitely required to gain benefit mind you, and
it
would appear that at least a few others on this list are unaware of
its
use and benefit. For the moment, I wish to address aspirin
specifically
and not ibuprofen. Although both are used for the same
purpose,
aspirin's use has been widely documented with respect to
decompression
diving. I submit the following to whomever for the sake
of
further discussion and intelligent hypothesis.
Aspirin
is a powerful medication and is actually an analgesic and
an
anti-inflammatory drug. Aspirin is a brand name in Canada;
acetylsalicylic
acid is the generic name. ASA, a commonly used
designation
for aspirin (or acetylsalicylic acid) in both the U.S. and
Canada,
is the term used in Canadian product labeling. Aspirin is an
over-the-counter
(OTC) medicine, and because it is so common and so
readily
available, many people do not consider it a "real medication."
This
is a common misconception and aspirin is a very "real drug." Its
use
in staged decompression diving has been extrapolated from other
benefits
that aspirin has been prescribed for (1).
Aspirin's
main use in diving is to prevent blood clotting and
platelet
aggregation. Although aspirin is referred to as a "blood
thinner,"
it does not actually "thin" the blood. Instead,
anticoagulants
alter proteins in the blood that are responsible for
clotting
while antiplatelet drugs prevent platelets from clumping and
forming
clots. Aspirin functions to make the platelets less 'sticky',
thereby
acting as an anti-coagulant. Aspirin is an aid; not a
substitute
for proper hydration, even though its main benefit to the
diver
is to allow improved blood flow and gas transport by increasing
tissue
gas perfusion.
In
vitro and in vivo studies have shown that hyperbaric pressure
increases
red blood cell (RBC) aggregation (2). Enhanced RBC
aggregation
in pathologic states can cause increased clotting. Both
aggregation
and clotting hamper the transport of gas which may lead to
any
number of hyperbaric related injuries.
It is known that the
hyper-aggregability
of platelets is remarkably important in the
pathogenesis
of decompression sickness (3).
One
investigation (2) examined the effects of pressure on RBC
aggregation
in human volunteers. The hypothesis tested was that RBC
aggregation
is increased during hyperbaric exposure. Subjects
participated
in dives to 300 fsw in a chamber. Blood samples were taken
at
the surface, at 66 fsw, and at 300 fsw. The median aggregate size
(number
of RBC/aggregate) of RBCs was significantly increased at depth.
The
deeper one goes, the greater the aggregate size. These results show
that
even mild pressure increases RBC aggregation in the human
circulation.
Therefore, aspirin is used as a preventive measure to a
known
prohibitor of gas transport, which may lead to symptomatic DCS.
There
are some controversial lines within the diving community
concerning
the use of aspirin. All groups are aware of the later; the
segregation
comes from discussion of aspirins effect on blood
viscosity.
There are some who contend that aspirin will reduce blood
viscosity
and therefore do more harm than good. Reduced blood viscosity
would
reduce gas tensions and therefore contribute to micro bubble
formation.
It
is unproven however, that aspirin will decrease the viscosity of
blood
and contribute to micro bubble formation.
Decreases in systemic
hematocrit
(blood count of red cells) tend to decrease blood viscosity
and
promote microvascular vasomotion and tissue perfusion (4,5), whereas
an
abnormally high hematocrit increases blood viscosity and results in
clumping
and aggregation of the erythrocytes, capillary occlusion and
regional
redistribution of the circulation.
One
study (6) examined the effects of aspirin and dipyridamole
(pronounced
dye-peer-id-a-mole -- its a powerful platelet aggregation
inhibitor;
antithrombotic adjunct) on platelet function, hematology, and
blood
chemistry of saturation divers. 24 divers were assigned randomly
to
4 treatment groups. Group I received aspirin (325
mg)
t.i.d. (ter in die, Latin meaning 3 times a day); Group II received
dipyridamole
(75 mg) t.i.d.; and Group III received both drug regimens;
while
group IV received matching placebo.
Double-blind
procedures were followed. Treatment began 24-h prior
to
a 48-h saturation dive (inclusive of 17 hour decompression) and
continued
throughout and for 3 days after the dive. A post-dive
reduction
in circulating platelet count was observed in all groups,
except
the group that received aspirin only. Platelet survival was
shortened
in all treatment groups. Five cases of Type I DCS occurred
and
were treated by recompression, two in the aspirin plus dipyridamole
group,
two in the dipyridamole group, and one in the placebo group; none
in
the aspirin only group.
Blood chemistry and hematology profiles
showed
that divers with decompression sickness had elevated GOT
(glutamic
oxaloacetic transaminase), GPT (glutamic pyruvic
transaminase),
and CPK (creatinine phosphokinase is one of several
chemicals
usually released in the blood after a heart attack, an
increase
of this form of isoenzyme in the blood is a diagnostic clue to
tissue
damage). Divers with DCS had more elevated cholesterol and
triglyceride
levels, and greater reductions in platelet count, platelet
factor
4 and thrombin (an enzyme formed in the clotting) clotting time
than
most other subjects. Subjects receiving either aspirin or aspirin
plus
dipyridamole had fewer changes in these parameters. Failure of
aspirin
to potentiate, or add to, dipyridamole may be due to other
actions
of aspirin such as inhibition of prostacyclin (PGI2 )
synthesis.
(PGI2
, a prostaglandin, is formed mainly in the blood vessel walls and
slows
blood platelet clumping. Aspirin, in doses as little as 4 mg/kg
of
body weight, inhibits prostacyclin as well as thromboxane formation.
Prostaglandins
may induce or inhibit platelet aggregation and constrict
or
dilate blood vessels. For an in-depth overview on prostaglandin and
thromboxane
biosynthesis; the role of steroidal and non- steroidal
anti-inflammatory
drugs; the reader is referred to an excellent review
by
Smith et al (7) )
This
particular study (6) seems to favour the use of aspirin in a
hyperbaric
environment, however further studies of the role of
antiplatelet
drugs such as dipyridamole in decompression sickness may be
warranted.
These results indicate that the combination of aspirin and
dipyridamole
offers no measurable advantage over aspirin alone. This
study
also suggests that antiplatelet drugs such as dipyridamole may
actually
be a contra-indication for a hyperbaric environment.
Yet
another study examined the hematology and blood chemistry in
saturation
diving using antiplatelet drugs, aspirin, and VK744. Blood
chemistry
and cellular parameters were studied before, during, and after
saturation
dives in a habitat, on two separate occasions. The results
confirm
previous observations and indicate that
post-decompression
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.
Lastly,
it should be stated that in vitro and in vivo research
clearly
demonstrates the influence of nutrition on platelet aggregation
and
clumping ie. eating fatty foods compounds the problematic blood
chemistry
situation (8-11).
Aspirin
is effectively used by many staged decompression divers who
can
tolerate the drugs side effects. In general, sustained release
doses
by divers, range from 325 mg to 600 mg, (single one time dose)
taken
60 to 120 minutes before a dive. There does not appear to be a
specific
or "magic" dose to provide for the best protection with the
least
amount of side effects. The anti-aggregating therapy usually
associated
with hyperbaric treatment involves administration of
acetylsalicylic
acid in low doses; 3.5 ~ 5 mg/kg of body weight (3).
During
one study (12), platelet functions were studied after
various
single doses of aspirin (75 mg, 150 mg, 300 mg, and 600 mg) in
20
males. Clotting time and platelet counts remained unchanged.
Significant
de-aggregation of platelets occurred only with 600 mg of
aspirin.
Another study (13) by Heavey et al, reports that an oral dose
of
aspirin (600 mg) causes rapid and substantial inhibition of
bradykinin-stimulated
PGI2 production, but recovery occurs within 6
hours;
this implies that endothelial PGI2 synthesis would be spared most
of
the time during dosing once daily with even this relatively large
dose
of aspirin (13).
Yet
another study (14), examined the effect of chronic
administration
of variable low doses of aspirin on platelet
adhesiveness,
platelet count, bleeding time and clotting time to find
out,
as to how low the dose of aspirin needs to be in order to have an
effective
antiplatelet effect in individuals who require such therapy
(meaning
over a longer period of time).
A statistically significant
reduction
in the platelet adhesiveness was observed in all the groups,
but
the best effect was exhibited by 50 mg of aspirin dose. Bleeding
time
was also increased in all the groups but statistically significant
difference
were observed with 50, 75 and 100 mg doses.
So
far we have doses somewhere between 50 mg/day, minium for long
term
chronic dosing; 325 mg t.i.d. for up to 5 days dosing (15); to 600
mg/day
one time minimum effective dosage. If one cares to search, they
will
find a myriad of studies for aspirin and effective dosages.
Therefore
it is next to impossible to give any hard line "best effect
dose"
which attains the best of aspirins benefits with the least amount
of
aspirin's side affects. There are several brands of coated aspirin
such
as 'Entrophen 10', an enteric coated tablet of ASA, which are
dissolved
in the gut instead of the stomach (650 mg effective for up to
six
hours or so). What is known however, is that antacids can decrease
the
effectiveness of aspirin.
Since
aspirin is an analgesic and an anti-inflammatory, where high
doses
are used, it may mask mild symptoms of DCS. Many antihystamines
and
corticosteriods used by divers for certain conditions, to aid in
ease
of equalization, can have the same effect. Excessive bleeding may
also
be a concern from an acquired injury such as cuts, bruises, broken
bones
etc. Bleeding into the middle ear or sinus from a squeeze may
require
special precaution as well. Every diver has minor trauma that
is
usually of little consequence. This can become a major problem if
the
diver is on perscription anticoagulants, however most authorities
(Bove,
Davis, DAN, etc.) agree that divers taking coumadin or other
anticoagulants
is either a relative contra-indication or an absolute
contraindication
to diving and therefore not an issue (16).
As well,
aspirin
may have more benefits to the decompression diver, with less
side
effects than those of anticoagulant drugs such as coumadin,
dipyridamole,
heparin etc.
The
added side bonus of aspirin in deep diving is of course, that
it
helps prevent pain associated with CO2 headaches commonly attributed
to
hard work and/or improper breathing techniques underwater. In short,
headache
is a sign that something is not right, however it's
not
a sure sign of CO2 buildup. The need for proper, slow,
moderate-sized
deep breathing technique during extreme depth diving
cannot
be overstated mind you.
Randy
F. Milak
(1)
Popovic P, et al. Levodopa and aspirin pretreatment beneficial in
experimental
decompression sickness. Proc Soc Exp Biol Med. 1982
Jan;169(1):140-3.
(2)
Taylor WF., Chen S, Barshtein G, Hyde DE, Yedgar S. Enhanced
aggregability
of human red blood cells by diving. Undersea Hyper Med
1998;
25(3)167-170.
(3)
Reggiani E, et al. Blood coagulation processes in decompression
sickness
and hyperbaric therapy. Minerva Med. 1981 May
31;72(22):1383-90.
(4)
Messmer K. Blood rheology factors and capillary blood flow, in
Gutierrez
G, Vincent JL (eds). Update in Intensive Care and Emergency
Medicine,
Vol 12, Tissue Oxygen Utilization. New York, Springer-Verlag,
1991,
pp 103-113.
(5)
Restorff WV, Hofling B, Holtz J, et al. Effect of increased blood
fluidity
through hemodilution on general circulation at rest and during
exercise
in dogs. Pflugers Arch 1975; 357: 25-34.
(6)
Philp RB, Bennett PB, Andersen JC, Fields GN, McIntyre BA, Francey
I,
Briner W. Effects of aspirin and dipyridamole on platelet function,
hematology,
and blood chemistry of saturation divers. Undersea Biomed
Res
1979 Jun;6(2):127-46
(7)
Smith WL, et al. Prostaglandin and thromboxane biosynthesis.
Pharmacol
Ther. 1991;49(3):153-79. Review.
(8)
Adam O, et al. Platelet aggregation and prostaglandin turnover in
man
during defined linoleic acid supply with formula diets. Res Exp Med
(Berl).
1980;177(3):227-35.
(9)
Temme EH, et al. Individual saturated fatty acids and effects on
whole
blood aggregation in vitro. Eur J Clin Nutr. 1998 Oct; 52
(10)
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