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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) )

		RANDOM PHOTOS

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) )
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This article was contributed by Mark Ellyatt, owner of Inspired-Training.com and author of the book Ocean Gladiator and can be contacted through his website or by email. The articles presented here do not necessarily reflect the beliefs and/or opinions of SDTechDiving; they are the sole written opinion/expression of the authors. SDTechDiving is not responsible for content contained within this article, including links which may take the reader to websites outside of our control.