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补充抗坏血酸可减轻水肺潜水后的微粒升高和中性粒细胞激活。

Ascorbic acid supplementation diminishes microparticle elevations and neutrophil activation following SCUBA diving.

作者信息

Yang Ming, Barak Otto F, Dujic Zeljko, Madden Dennis, Bhopale Veena M, Bhullar Jasjeet, Thom Stephen R

机构信息

Department of Emergency Medicine, University of Maryland School of Medicine, Baltimore, Maryland; and.

Department of Physiology, University of Split School of Medicine, Split, Croatia.

出版信息

Am J Physiol Regul Integr Comp Physiol. 2015 Aug 15;309(4):R338-44. doi: 10.1152/ajpregu.00155.2015. Epub 2015 Jun 17.

DOI:10.1152/ajpregu.00155.2015
PMID:26084697
Abstract

Predicated on evidence that diving-related microparticle generation is an oxidative stress response, this study investigated the role that oxygen plays in augmenting production of annexin V-positive microparticles associated with open-water SCUBA diving and whether elevations can be abrogated by ascorbic acid. Following a cross-over study design, 14 male subjects ingested placebo and 2-3 wk later ascorbic acid (2 g) daily for 6 days prior to performing either a 47-min dive to 18 m of sea water while breathing air (∼222 kPa N2/59 kPa O2) or breathing a mixture of 60% O2/balance N2 from a tight-fitting face mask at atmospheric pressure for 47 min (∼40 kPa N2/59 kPa O2). Within 30 min after the 18-m dive in the placebo group, neutrophil activation, and platelet-neutrophil interactions occurred, and the total number of microparticles, as well as subgroups bearing CD66b, CD41, CD31, CD142 proteins or nitrotyrosine, increased approximately twofold. No significant elevations occurred among divers after ingesting ascorbic acid, nor were elevations identified in either group after breathing 60% O2. Ascorbic acid had no significant effect on post-dive intravascular bubble production quantified by transthoracic echocardiography. We conclude that high-pressure nitrogen plays a key role in neutrophil and microparticle-associated changes with diving and that responses can be abrogated by dietary ascorbic acid supplementation.

摘要

基于与潜水相关的微粒生成是一种氧化应激反应的证据,本研究调查了氧气在增加与开放水域水肺潜水相关的膜联蛋白V阳性微粒产生中所起的作用,以及这种增加是否可以被抗坏血酸消除。采用交叉研究设计,14名男性受试者先摄入安慰剂,2至3周后,在进行47分钟潜水至18米海水深度(呼吸空气,约222 kPa氮气/59 kPa氧气)或在常压下通过紧密贴合的面罩呼吸60%氧气/其余为氮气的混合气体47分钟(约40 kPa氮气/59 kPa氧气)之前,每天摄入抗坏血酸(2克),持续6天。在安慰剂组进行18米潜水后的30分钟内,中性粒细胞活化以及血小板-中性粒细胞相互作用发生,微粒总数以及携带CD66b、CD41、CD31、CD142蛋白或硝基酪氨酸的亚组微粒数量增加了约两倍。摄入抗坏血酸后潜水者中未出现显著升高,呼吸60%氧气后两组中也未发现升高情况。抗坏血酸对通过经胸超声心动图量化的潜水后血管内气泡产生没有显著影响。我们得出结论,高压氮气在潜水引起的中性粒细胞和微粒相关变化中起关键作用,并且通过饮食补充抗坏血酸可以消除这些反应。

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