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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.

1. Randy F. Milak.
2. Popovic P, et al. Levodopa and aspirin pretreatment beneficial in experimental decompression sickness. Proc Soc Exp Biol Med. 1982 Jan;169(1):140-3.
3. 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.
4. Reggiani E, et al. Blood coagulation processes in decompression sickness and hyperbaric therapy. Minerva Med. 1981 May 31;72(22):1383-90.
5. 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.
6. 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.
7. 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.
8. Smith WL, et al. Prostaglandin and thromboxane biosynthesis. Pharmacol Ther. 1991;49(3):153-79. Review.
9. 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.
10. Temme EH, et al. Individual saturated fatty acids and effects on whole blood aggregation in vitro. Eur J Clin Nutr. 1998 Oct; 52

		RANDOM PHOTOS

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. 1. Randy F. Milak. 2. Popovic P, et al. Levodopa and aspirin pretreatment beneficial in experimental decompression sickness. Proc Soc Exp Biol Med. 1982 Jan;169(1):140-3. 3. 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. 4. Reggiani E, et al. Blood coagulation processes in decompression sickness and hyperbaric therapy. Minerva Med. 1981 May 31;72(22):1383-90. 5. 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. 6. 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. 7. 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. 8. Smith WL, et al. Prostaglandin and thromboxane biosynthesis. Pharmacol Ther. 1991;49(3):153-79. Review. 9. 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. 10. Temme EH, et al. Individual saturated fatty acids and effects on whole blood aggregation in vitro. Eur J Clin Nutr. 1998 Oct; 52
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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.