Suzuki S
Japan Maritime Self-Defense Force Undersea Medical Center, Yokosuka.
Undersea Hyperb Med. 1994 Sep;21(3):235-43.
To investigate the possibility of lung injury after long-term saturation dives where oxygen partial pressure was kept between 42 and 50 kPa, we measured lung volumes, diffusing capacity (DLCO/VA), and ethane production in the alveolar expirate on six divers who participated in a 1.1-MPa saturation dive (9 days of total dive time) and on another six divers in a 4.5-MPa saturation dive (29 days of total dive time). Vital capacity after surfacing did not significantly decrease in divers after either dive profile, in comparison with predive values. DLCO/VA was significantly decreased only in the 4.5-MPa saturation divers after surfacing. Ethane production, used as an index of in vivo lipid peroxidation, was significantly increased immediately after the 4.5-MPa saturation dive. The decompression procedure seemed to have little effect on the decrease in diffusing capacity and increase in ethane production. These observations indicated that the decrease of DLCO/VA was assumed to be caused by oxygen-derived free radicals.
为了研究在氧分压保持在42至50 kPa的长期饱和潜水后发生肺损伤的可能性，我们测量了参与1.1兆帕饱和潜水（总潜水时间9天）的6名潜水员以及参与4.5兆帕饱和潜水（总潜水时间29天）的另外6名潜水员的肺容积、弥散能力（DLCO/VA）和肺泡呼出物中的乙烷生成量。与潜水前的值相比，两种潜水方案后的潜水员浮出水面后的肺活量均未显著降低。仅在4.5兆帕饱和潜水的潜水员浮出水面后，DLCO/VA显著降低。用作体内脂质过氧化指标的乙烷生成量在4.5兆帕饱和潜水后立即显著增加。减压程序似乎对弥散能力的降低和乙烷生成量的增加影响很小。这些观察结果表明，DLCO/VA的降低被认为是由氧衍生的自由基引起的。
