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低压暴露下大鼠脂肪组织中气泡衰减和稳定的阈值高度。

Threshold altitude for bubble decay and stabilization in rat adipose tissue at hypobaric exposures.

作者信息

Randsoe Thomas, Hyldegaard Ole

机构信息

Laboratory of Hyperbaric Medicine, Department of Anaesthesia, Centre of Head and Orthopaedics, Rigshospitalet, University Hospital of Copenhagen, Copenhagen, Denmark.

出版信息

Aviat Space Environ Med. 2013 Jul;84(7):675-83. doi: 10.3357/asem.3489.2013.

Abstract

INTRODUCTION

Bubble formation during altitude exposures, causing altitude decompression sickness (aDCS), has been referred to in theoretical models as venous gas embolisms (VGE). This has also been demonstrated by intravascular gas formation. Previous reports indicate that the formation of VGE and aDCS incidence increase abruptly for exposures exceeding 40-44 kPa ambient pressures. Further, extravascular micro air bubbles injected into adipose tissue grow transiently, then shrink and disappear while breathing oxygen (F1O2 = 1.0) at 71 kPa. At 25 kPa similar air bubbles will grow and stabilize during oxygen breathing without disappearing. We hypothesize that an ambient pressure threshold for either extravascular bubble stabilization or disappearance may be identified between 71 and 25 kPa. Whether extravascular bubbles will stabilize above a certain threshold has not been demonstrated before.

METHODS

In anesthetized rats, micro air bubbles (containing 79% nitrogen) of 500 nl were injected into exposed abdominal adipose tissue. Rats were decompressed in 2-35 min to either 60, 47, or 36 kPa and bubbles studied for 215 min during continued oxygen breathing (F1O2 = 1).

RESULTS

Significantly more bubbles shrank and disappeared at 60 (14 of 17) and 47 kPa (14 of 15) as compared to bubbles exposed to 36 kPa (3 of 15) ambient pressure.

CONCLUSION

The results indicate that a threshold causing extravascular bubble stabilization or decay is between 47 to 36 kPa. The results are in agreement with previous reports demonstrating an increase in the formation of VGE and symptoms of aDCS at altitudes higher than 44 kPa ambient pressure.

摘要

引言

在高空暴露期间形成的气泡会导致高空减压病(aDCS),在理论模型中被称为静脉气体栓塞(VGE)。血管内气体形成也证实了这一点。先前的报告表明,当暴露于超过40 - 44 kPa的环境压力时,VGE的形成和aDCS的发病率会突然增加。此外,注入脂肪组织的血管外微气泡会短暂生长,然后在71 kPa下呼吸氧气(F1O2 = 1.0)时收缩并消失。在25 kPa时,类似的气泡在吸氧过程中会生长并稳定下来,不会消失。我们假设在71 kPa至25 kPa之间可能存在血管外气泡稳定或消失的环境压力阈值。此前尚未证明血管外气泡是否会在某个阈值以上稳定下来。

方法

在麻醉的大鼠中,将500 nl含79%氮气的微气泡注入暴露的腹部脂肪组织。大鼠在2 - 35分钟内减压至60、47或36 kPa,并在持续吸氧(F1O2 = 1)的过程中对气泡进行215分钟的研究。

结果

与暴露于36 kPa环境压力的气泡(15个中有3个)相比,在60 kPa(17个中有14个)和47 kPa(15个中有14个)时,明显更多的气泡收缩并消失。

结论

结果表明,导致血管外气泡稳定或衰减的阈值在47至36 kPa之间。该结果与先前的报告一致,这些报告表明在高于44 kPa环境压力的高空,VGE的形成和aDCS的症状会增加。

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