Thorsen E, Segadal K, Stuhr L E B, Troland K, Grønning M, Marstein S, Hope A
Institute of Medicine, University of Bergen, Bergen, Norway.
Eur J Appl Physiol. 2006 Oct;98(3):270-5. doi: 10.1007/s00421-006-0276-8. Epub 2006 Sep 9.
Decompression stress and exposure to hyperoxia may cause a reduction in transfer factor of the lung for carbon monoxide and in maximal aerobic capacity after deep saturation dives. In this study lung function and exercise capacity were assessed before and after a helium-oxygen saturation dive to a pressure of 2.5 MPa where the decompression rate was reduced compared with previous deep dives, and the hyperoxic exposure was reduced by administering oxygen intermittently at pressures of 50 and 30 kPa during decompression. Eight experienced divers of median age 41 years (range 29-48) participated in the dive. The incidence of venous gas microemboli was low compared with previous deep dives. Except for one subject having treatment for decompression sickness, no changes in lung function or angiotensin converting enzyme, a marker of pulmonary endothelial cell damage, were demonstrated. The modified diving procedures with respect to decompression rate and hyperoxic exposure may have contributed to the lack of changes in lung function in this dive compared with previous deep saturation dives.
减压应激和高氧暴露可能会导致深度饱和潜水后肺一氧化碳转运因子和最大有氧能力降低。在本研究中,对8名有经验的潜水员进行了氦氧饱和潜水,潜水深度达2.5兆帕,与之前的深度潜水相比,减压速率降低,并且在减压过程中通过在50千帕和30千帕压力下间歇性供氧来减少高氧暴露,分别在潜水前后评估了他们的肺功能和运动能力。这8名潜水员年龄中位数为41岁(范围29 - 48岁)。与之前的深度潜水相比,静脉气体微栓子的发生率较低。除一名接受减压病治疗的受试者外,未发现肺功能或肺血管内皮细胞损伤标志物血管紧张素转换酶有变化。与之前的深度饱和潜水相比,本次潜水在减压速率和高氧暴露方面采用的改良潜水程序可能是肺功能未发生变化的原因。