Lambrechts Kate, Pontier Jean-Michel, Mazur Aleksandra, Buzzacott Peter, Goanvec Christelle, Wang Qiong, Theron Michaël, Belhomme Marc, Guerrero François
Orphy 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, E-mail:
Diving and Hyperbaric Department, French Navy Diving School, Brest, France.
Diving Hyperb Med. 2014 Sep;44(3):154-7.
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.
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.
There were no differences between the groups in DCS outcome or in PF4, TBARS and VWf concentrations.
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.
脾脏血小板已被认为比其他血小板具有更大的促血栓形成潜力。我们研究了脾脏收缩释放的血小板是否会影响减压病(DCS)的严重程度和结局以及气泡诱导的血小板活化。
将16只雄性Sprague-Dawley大鼠随机分为对照组或脾切除组。两组在分级减压前(在200 kPa下5分钟、在160 kPa下5分钟和在130 kPa下10分钟)呼吸空气时均被压缩至1000 kPa(90米海水)45分钟。在潜水后60分钟的观察期内记录DCS症状和死亡的发作时间。测量的参数包括用于血小板活化的血小板因子4(PF4)、用于氧化应激状态的硫代巴比妥酸反应性物质(TBARS)和用于内皮活化的血管性血友病因子(VWf)。
两组在DCS结局或PF4、TBARS和VWf浓度方面没有差异。
这些结果不支持在大鼠模型中脾脏及其可交换血小板池参与DCS发病机制,这使得减压诱导的血小板聚集增加可能受脾脏收缩影响并进而在DCS结局中起作用这一假设无效。