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I can pretty much guarantee that some members of this board take it. I can absolutely guarantee that a number of active divers take it.
I posted this some years ago:
"J Appl Physiol. 2011 Jan 6. [Epub ahead of print]
Pharmacological intervention against bubble-induced platelet aggregation in a rat model of decompression sickness.
Pontier JM, Vallee N, Ignatescu M, Bourdon L.
1 Naval Medical Institute.
Abstract
Decompression sickness (DCS) with alterations in coagulation system and formation of platelet thrombi occurs when a subject is subjected to a reduction in environmental pressure. Blood platelet consumption after decompression is clearly linked to bubble formation in humans and offers an index for evaluating DCS severity in animal models. Previous studies highlighted a predominant involvement of platelet activation and thrombin generation in bubble-induced platelet aggregation. In order to study the mechanism of the bubble-induced platelet aggregation in DCS, we examined the effect of acetylsalicylic acid (ASA), heparin (Hep) and clopidogrel (Clo), with anti-thrombotic dose pre-treatment in a rat model of decompression sickness. Male Sprague-Dawley rats were first compressed to 1000 kPa for 45 min then decompressed to surface in 38 min. In a control experiment, rats were treated with ASA, Clo, or Hep, and maintained at atmospheric pressure for an equivalent period of time. Onset of DCS symptoms and death were recorded during a 60-min observation period after surfacing. DCS evaluation included pulmonary and neurological signs. Blood samples for platelet count (PC) were taken before hyperbaric exposure and after surfacing. Clopidogrel reduces the DCS mortality risk and DCS severity. Clopidogrel reduced fall in platelet count and bubble-induced platelet aggregation (-4,5% with Clo, - 19.5% with ASA, -19,9% with Hep and -29,6% in the untreated group). ASA which inhibits the thromboxane A2 pathway and Hep which inhibits thrombin generation have no protective effect on DCS incidence. Clopidogrel, a specific ADP-receptor antagonist, reduces post-decompression platelet consumption. These results point to the predominant involvement of the ADP release in bubble-induced platelet aggregation but cannot differentiate definitively between bubble-induced vessel wall injury and bubble-blood component interactions in DCS."
In the latest published research we're still in the rat model, for somewhat understandable reasons, but the findings remain encouraging:
"Respir Physiol Neurobiol. 2015 Jun;211:9-16. doi: 10.1016/j.resp.2015.02.003. Epub 2015 Mar 14.
Clopidogrel reduces the inflammatory response of lung in a rat model of decompression sickness.
Bao XC1, Chen H2, Fang YQ3, Yuan HR1, You P1, Ma J1, Wang FF1.
Abstract
Inflammation and platelet activation are critical phenomena in the setting of decompression sickness. Clopidogrel (Clo) inhibits platelet activation and may also reduce inflammation. The goal of this study was to investigate if Clo had a protective role in decompression sickness (DCS) through anti-inflammation way. Male Sprague-Dawley rats (n=111) were assigned to three groups: control+vehicle group, DCS+vehicle, DCS+Clo group. The experimental group received 50mg/kg of Clo or vehicle for 3 days, then compressed to 1,600kPa (150msw) in 28s, maintained at 150msw for 242s and decompressed to surface at 3m/s. In a control experiment, rats were also treated with vehicle for 3 days and maintained at atmospheric pressure for an equivalent period of time. Clinical assessment took place over a period of 30min after surfacing. At the end, blood samples were collected for blood cells counts and cytokine detection. The pathology and the wet/dry ratio of lung tissues, immunohistochemical detection of lung tissue CD41 expression, the numbers of P-selectin positive platelets and platelet-leukocyte conjugates in blood were tested. We found that Clo significantly reduced the DCS mortality risk (mortality rate: 11/45 with Clo vs. 28/46 in the untreated group, P<0.01). Clo reduced the lung injury, the wet/dry ratio of lung, the accumulation of platelet and leukocyte in lung, the fall in platelet count, the WBC count, the numbers of activated platelets and platelet-leukocyte complexes in peripheral blood. It was concluded that Clo can play a protective role in decompression sickness through reducing post-decompression platelet activation and inflammatory process."
Cheers,
DocVikingo
I posted this some years ago:
"J Appl Physiol. 2011 Jan 6. [Epub ahead of print]
Pharmacological intervention against bubble-induced platelet aggregation in a rat model of decompression sickness.
Pontier JM, Vallee N, Ignatescu M, Bourdon L.
1 Naval Medical Institute.
Abstract
Decompression sickness (DCS) with alterations in coagulation system and formation of platelet thrombi occurs when a subject is subjected to a reduction in environmental pressure. Blood platelet consumption after decompression is clearly linked to bubble formation in humans and offers an index for evaluating DCS severity in animal models. Previous studies highlighted a predominant involvement of platelet activation and thrombin generation in bubble-induced platelet aggregation. In order to study the mechanism of the bubble-induced platelet aggregation in DCS, we examined the effect of acetylsalicylic acid (ASA), heparin (Hep) and clopidogrel (Clo), with anti-thrombotic dose pre-treatment in a rat model of decompression sickness. Male Sprague-Dawley rats were first compressed to 1000 kPa for 45 min then decompressed to surface in 38 min. In a control experiment, rats were treated with ASA, Clo, or Hep, and maintained at atmospheric pressure for an equivalent period of time. Onset of DCS symptoms and death were recorded during a 60-min observation period after surfacing. DCS evaluation included pulmonary and neurological signs. Blood samples for platelet count (PC) were taken before hyperbaric exposure and after surfacing. Clopidogrel reduces the DCS mortality risk and DCS severity. Clopidogrel reduced fall in platelet count and bubble-induced platelet aggregation (-4,5% with Clo, - 19.5% with ASA, -19,9% with Hep and -29,6% in the untreated group). ASA which inhibits the thromboxane A2 pathway and Hep which inhibits thrombin generation have no protective effect on DCS incidence. Clopidogrel, a specific ADP-receptor antagonist, reduces post-decompression platelet consumption. These results point to the predominant involvement of the ADP release in bubble-induced platelet aggregation but cannot differentiate definitively between bubble-induced vessel wall injury and bubble-blood component interactions in DCS."
In the latest published research we're still in the rat model, for somewhat understandable reasons, but the findings remain encouraging:
"Respir Physiol Neurobiol. 2015 Jun;211:9-16. doi: 10.1016/j.resp.2015.02.003. Epub 2015 Mar 14.
Clopidogrel reduces the inflammatory response of lung in a rat model of decompression sickness.
Bao XC1, Chen H2, Fang YQ3, Yuan HR1, You P1, Ma J1, Wang FF1.
Abstract
Inflammation and platelet activation are critical phenomena in the setting of decompression sickness. Clopidogrel (Clo) inhibits platelet activation and may also reduce inflammation. The goal of this study was to investigate if Clo had a protective role in decompression sickness (DCS) through anti-inflammation way. Male Sprague-Dawley rats (n=111) were assigned to three groups: control+vehicle group, DCS+vehicle, DCS+Clo group. The experimental group received 50mg/kg of Clo or vehicle for 3 days, then compressed to 1,600kPa (150msw) in 28s, maintained at 150msw for 242s and decompressed to surface at 3m/s. In a control experiment, rats were also treated with vehicle for 3 days and maintained at atmospheric pressure for an equivalent period of time. Clinical assessment took place over a period of 30min after surfacing. At the end, blood samples were collected for blood cells counts and cytokine detection. The pathology and the wet/dry ratio of lung tissues, immunohistochemical detection of lung tissue CD41 expression, the numbers of P-selectin positive platelets and platelet-leukocyte conjugates in blood were tested. We found that Clo significantly reduced the DCS mortality risk (mortality rate: 11/45 with Clo vs. 28/46 in the untreated group, P<0.01). Clo reduced the lung injury, the wet/dry ratio of lung, the accumulation of platelet and leukocyte in lung, the fall in platelet count, the WBC count, the numbers of activated platelets and platelet-leukocyte complexes in peripheral blood. It was concluded that Clo can play a protective role in decompression sickness through reducing post-decompression platelet activation and inflammatory process."
Cheers,
DocVikingo
