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Effect of splenectomy on platelet activation and decompression sickness outcome in a rat model of decompression
Kate Lambrechts1, Jean-Michel Pontier2, Aleksandra Mazur3
1Orphy Laboratory, Université de Bretagne Occidentale, EA 4324 - Optimisation des Régulations Physiologique UFR Sciences et Techniques, 6 avenue Le Gorgeu, CS 93837, Brest Cedex 3, France, Phone: +33 (7) 62 14 11 60, Fax: +33 (2) 98 01 63 11,
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.
