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暴露于8个绝对大气压、温度在10至35摄氏度环境下的大鼠体内的氮负荷不会影响减压病风险。

Nitrogen load in rats exposed to 8 ATA from 10-35 degrees C does not influence decompression sickness risk.

作者信息

Fahlman Andreas, Kayar Susan R

机构信息

Diving and Environmental Physiology Department, Naval Medical Research Center, Silver Spring, MD, USA.

出版信息

Aviat Space Environ Med. 2006 Aug;77(8):795-800.

Abstract

INTRODUCTION

Environmental temperature is commonly thought to modulate decompression sickness (DCS) risk, but the literature is mixed regarding which conditions elicit the greatest risk. If temperature is a risk factor, then managing thermal exposure may reduce DCS incidence. We analyzed whether hot or cold conditions during or immediately after a hyperbaric exposure altered DCS incidence in a rat model.

METHODS

Rats (eight groups of five animals in each of nine conditions; mean body mass +/- SD = 259.0 +/- 9.2 g) were placed in a dry chamber that was pressurized with air to 70 m (8 ATA) for 25 min, followed by rapid (< 30 s) decompression under a series of temperature conditions (35 degrees, 27 degrees, or 10 degrees C during compression; 35 degrees, 20 degrees, or 10 degrees C post-decompression). Animals were observed for 30 min post-decompression for signs of DCS. DCS incidence in the 27 degrees C compression/20 degrees C post-decompression group was 50% by design. Data from all nine groups of paired temperature conditions were compared with each other using analysis of variance, Chi-square tests, and logistic regression.

RESULTS

No significant differences in DCS incidence were found among the groups (30-52.5% DCS incidence per group, 42% DCS incidence overall).

DISCUSSION AND CONCLUSIONS

This animal model emphasized potential temperature effects attributable to tissue N2 load acquired during compression; there was no evidence that environmental temperature from 10-35 degrees C during or post-dive modulated DCS incidence. It remains to be determined if temperature modulates DCS risk as a function of variable N2 elimination rates.

摘要

引言

环境温度通常被认为会调节减压病(DCS)风险,但关于哪种条件会引发最大风险,文献中的观点并不一致。如果温度是一个风险因素,那么控制热暴露可能会降低DCS的发病率。我们分析了在高压暴露期间或之后立即处于热或冷的条件下,是否会改变大鼠模型中DCS的发病率。

方法

将大鼠(9种条件下每组8组,每组5只动物;平均体重+/-标准差=259.0+/-9.2克)置于一个干燥舱中,用空气加压至70米(8个绝对大气压)并保持25分钟,然后在一系列温度条件下(压缩期间为35℃、27℃或10℃;减压后为35℃、20℃或10℃)进行快速(<30秒)减压。在减压后观察动物30分钟,观察是否有DCS的迹象。27℃压缩/20℃减压后组的DCS发病率按设计为50%。使用方差分析、卡方检验和逻辑回归对所有9组配对温度条件的数据进行相互比较。

结果

各组之间的DCS发病率没有显著差异(每组DCS发病率为30%-52.5%,总体DCS发病率为42%)。

讨论与结论

该动物模型强调了压缩过程中获得的组织氮气负荷可能产生的温度效应;没有证据表明潜水期间或之后10-35℃的环境温度会调节DCS发病率。温度是否作为可变氮气消除率的函数来调节DCS风险仍有待确定。

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