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    Effect of splenectomy on platelet activation and decompression sickness outcome in a rat model of decompression

    Access Status
    Fulltext not available
    Authors
    Lambrechts, K.
    Pontier, J.
    Mazur, A.
    Buzzacott, Peter
    Goanvec, C.
    Wang, Q.
    Theron, M.
    Belhomme, M.
    Guerrero, F.
    Date
    2014
    Type
    Journal Article
    
    Metadata
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    Citation
    Lambrechts, K. and Pontier, J. and Mazur, A. and Buzzacott, P. and Goanvec, C. and Wang, Q. and Theron, M. et al. 2014. Effect of splenectomy on platelet activation and decompression sickness outcome in a rat model of decompression. Diving and Hyperbaric Medicine. 44 (3): pp. 154-157.
    Source Title
    Diving and Hyperbaric Medicine
    ISSN
    1833-3516
    School
    School of Nursing, Midwifery and Paramedicine
    URI
    http://hdl.handle.net/20.500.11937/72223
    Collection
    • Curtin Research Publications
    Abstract

    © 2014, South Pacific Underwater Medicine Society. All rights reserved. Introduction: Splenic platelets have been recognized to have a greater prothrombotic potential than others platelets. We studied whether platelets released by splenic contraction could influence the severity and outcome of decompression sickness (DCS) and bubble-induced platelet activation. Methods: Sixteen, male Sprague-Dawley rats were randomly assigned to either a control or a splenectomized group. Both groups were compressed to 1,000 kPa (90 metres’ sea water) for 45 min while breathing air before staged decompression (5 min at 200 kPa, 5 min at 160 kPa and 10 min at 130 kPa). The onset time of DCS symptoms and of death were recorded during a 60-min observation period post dive. Parameters measured were platelet factor 4 (PF4) for platelet activation, thiobarbituric acid reactive substances (TBARS) for oxidative stress status and Von Willebrand factor (VWf) for endothelial activation. Results: There were no differences between the groups in DCS outcome or in PF4, TBARS and VWf concentrations. Conclusion: These results do not support that the spleen and its exchangeable platelet pool is involved in DCS pathogenesis in a rat model, invalidating the hypothesis that increased decompression-induced platelet aggregation could be influenced by splenic contraction and then play a role in DCS outcome.

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