Department of Emergency Medicine, University of California San Diego, La Jolla, CA, United States of America.
Department of Radiology, University of California San Diego, La Jolla, CA, United States of America.
PLoS One. 2024 Jan 22;19(1):e0294611. doi: 10.1371/journal.pone.0294611. eCollection 2024.
Breathing pure oxygen causes nitrogen washout from tissues, a method commonly deployed to prevent decompression sickness from hypobaric exposure. Theoretically prebreathing oxygen increases the capacity for nitrogen uptake and potentially limits supersaturation during dives of short duration. We aimed to use 13N2, a radioactive nitrogen isotope, to quantify tissue nitrogen following normobaric and hyperbaric exposures.
Twenty Sprague Dawley rats were divided in 4 conditions; normobaric prebreathe, normobaric control, hyperbaric prebreathe, hyperbaric control. Prebreathed rats breathed oxygen for 1 h prior to the experiment whilst controls breathed air. Normobaric rats breathed air containing 13N2 at 100 kPa for 30 min, whereas hyperbaric rats breathed 13N2 at 700 kPa before being decompressed and sedated using air-isoflurane (without 13N2 for a few minutes). After euthanization, blood, brain, liver, femur and thigh muscle were analyzed by gamma counting.
At normobaria prebreathing oxygen resulted in higher absolute nitrogen counts in blood (p = .034), as well as higher normalized counts in both the liver and muscle (p = .034). However, following hyperbaric exposure no differences were observed between conditions for any organ (p>.344). Both bone and muscle showed higher normalized counts after hyperbaria compared to normobaria.
Oxygen prebreathing caused nitrogen elimination in normobaria that led to a larger "sink" and uptake of 13N2. The lack of difference between conditions in hyperbaria could be due to the duration and depth of the dive mitigating the effect of prebreathing. In the hyperbaric conditions the lower counts were likely due to off-gassing of nitrogen during the sedation procedure, suggest a few minutes was enough to off-gas in rodents. The higher normalized counts under hyperbaria in bone and muscle likely relate to these tissues being slower to on and off-gas nitrogen. Future experiments could include shorter dives and euthanization while breathing 13N2 to prevent off-gassing.
呼吸纯氧会导致组织中的氮气排出,这是一种常用于预防低压暴露引起减压病的方法。理论上,预吸氧会增加氮气摄取能力,并在短时间潜水时限制过饱和。我们旨在使用放射性氮同位素 13N2 来量化常压和高压暴露后的组织氮含量。
将 20 只 Sprague Dawley 大鼠分为 4 种情况:常压预吸氧、常压对照、高压预吸氧、高压对照。预吸氧组大鼠在实验前吸氧 1 小时,而对照组大鼠呼吸空气。常压组大鼠在 100 kPa 下呼吸含 13N2 的空气 30 分钟,而高压组大鼠在 700 kPa 下呼吸 13N2 后减压并使用空气异氟烷镇静(几分钟内无 13N2)。安乐死后,通过伽马计数分析血液、大脑、肝脏、股骨和大腿肌肉。
在常压下,预吸氧导致血液中绝对氮计数升高(p =.034),肝脏和肌肉中的归一化计数也升高(p =.034)。然而,在高压暴露后,任何器官的条件之间都没有差异(p>.344)。与常压相比,高压后骨骼和肌肉的归一化计数更高。
常压下的预吸氧导致氮气在常压下的消除,从而形成更大的“氮吸收池”并吸收 13N2。高压下条件之间没有差异可能是由于潜水的持续时间和深度减轻了预吸氧的影响。在高压条件下,计数较低可能是由于镇静过程中氮气的逸出,提示在啮齿动物中几分钟就足以逸出氮气。高压下骨骼和肌肉中归一化计数较高可能与这些组织较慢地吸收和释放氮气有关。未来的实验可以包括更短的潜水和在呼吸 13N2 时安乐死,以防止氮气逸出。