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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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