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首页> 外文期刊>European journal of applied physiology >Effect of oxygen-breathing during a decompression-stop on bubble-induced platelet activation after an open-sea air dive: Oxygen-stop decompression
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Effect of oxygen-breathing during a decompression-stop on bubble-induced platelet activation after an open-sea air dive: Oxygen-stop decompression

机译:减压期间氧气呼吸的影响 - 张开海上空气潜水后血泡诱导的血小板活化:氧气停止减压

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Purpose: We highlighted a relationship between decompression-induced bubble formation and platelet micro-particle (PMP) release after a scuba air-dive. It is known that decompression protocol using oxygen-stop accelerates the washout of nitrogen loaded in tissues. The aim was to study the effect of oxygen deco-stop on bubble formation and cell-derived MP release. Methods: Healthy experienced divers performed two scuba-air dives to 30 msw for 30 min, one with an air deco-stop and a second with 100 % oxygen deco-stop at 3 msw for 9 min. Bubble grades were monitored with ultrasound and converted to the Kisman integrated severity score (KISS). Blood samples for cell-derived micro-particle analysis (AnnexinV for PMP and CD31 for endothelial MP) were taken 1 h before and after each dive. Results: Mean KISS bubble score was significantly lower after the dive with oxygen-decompression stop, compared to the dive with air-decompression stop (4.3 ± 7.3 vs. 32.7 ± 19.9, p < 0.001). After the dive with an air-breathing decompression stop, we observed an increase of the post-dive mean values of PMP (753 ± 245 vs. 381 ± 191 ng/μl, p = 0.003) but no significant change in the oxygen-stop decompression dive (329 ± 215 vs. 381 +/191 ng/μl, p = 0.2). For the post-dive mean values of endothelial MP, there was no significant difference between both the dives. Conclusions: The Oxygen breathing during decompression has a beneficial effect on bubble formation accelerating the washout of nitrogen loaded in tissues. Secondary oxygen-decompression stop could reduce bubble-induced platelet activation and the pro-coagulant activity of PMP release preventing the thrombotic event in the pathogenesis of decompression sickness.
机译:目的:在水肺气候后,突出了减压诱导的泡沫形成和血小板微粒(PMP)释放的关系。众所周知,使用氧气止动术的减压协议加速了组织中加载的氮气的冲洗。目的是研究氧气输液对气泡形成和细胞衍生MP释放的影响。方法:健康经验丰富的潜水员在30 msw中进行了30分钟,一个空气地止挡,一秒钟,氧气10%在3ms 3mst 9分钟。用超声监测泡沫等级并转换为Kisman综合严重性评分(吻)。每次潜水之前和之后,在1小时内完成用于细胞衍生的微粒分析的血液样品(用于预型MP的PMP和CD31)。结果:平均接吻泡沫分数在潜水缓冲止动液后潜水显着较低,与空气减压止动(4.3±7.3与32.7±19.9,P <0.001)相比。潜水后呼吸减压停止后,我们观察到PMP后潜水平均值的增加(753±245与381±191 ng /μl,p = 0.003),但氧气停止没有显着变化减压潜水(329±215 vs.381 + / 191 ng /μl,p = 0.2)。对于内皮MP的后潜力平均值,潜水之间没有显着差异。结论:减压期间的氧气呼吸对气泡形成的有益作用,加速了组织中含有的氮气的冲洗。二次氧气减压止动可降低血泡诱导的血小板活化和PMP释放的促凝血活性,防止血栓形成事件在减压病的发病机制中。

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