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Effects of scuba diving on vascular repair mechanisms

机译:潜水对血管修复的影响机制

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摘要

A single air dive causes transient endothelial dysfunction. Endothelial progenitor cells (EPCs) and circulating angiogenic cells (CAC) contribute synergistically to endothelial repair. In this study (1) the acute effects of diving on EPC numbers and CAC migration and (2) the influence of the gas mixture (air/nitrox-36) was investigated. Ten divers performed two dives to 18 meters on Day (D) 1 and D3, using air. After 15 days, dives were repeated with nitrox-36. Blood sampling took place before and immediately after diving. Circulating EPCs were quantified by flow cytometry, CAC migration of culture was assessed on D7. When diving on air, a trend for reduced EPC numbers is observed post-dive, which is persistent on D1 and D3. CAC migration tends to improve acutely following diving. These effects are more pronounced with nitrox-36 dives. Diving acutely affects EPC numbers and CAC function, and to a larger extent when diving with nitrox-36. The diving-induced oxidative stress may influence recruitment or survival of EPC. The functional improvement of CAC could be a compensatory mechanism to maintain endothelial homeostasis.
机译:一个空气潜水导致瞬态内皮功能障碍。和循环血管生成细胞(CAC)贡献是为内皮修复。研究(1)急性潜水对EPC的影响数字和CAC迁移和(2)的影响的气体混合物(空气/ nitrox-36)调查。18米(D) 1天,D3,使用空气。15天,潜水与nitrox-36重复。血液采样并立即之前发生后潜水。流式细胞术,CAC移民文化评估D7。EPC数量减少是观察潜水后,持续在D1和D3。改善后敏锐地潜水。与nitrox-36潜水效应更加明显。潜水严重影响EPC号码和CAC功能,更大程度上潜水时nitrox-36。可能影响招聘或EPC的生存。功能改进CAC的可能代偿机制维持内皮体内平衡。

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