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首页> 美国卫生研究院文献>Springer Open Choice >Effect of isobaric breathing gas shifts from air to heliox mixtures on resolution of air bubbles in lipid and aqueous tissues of recompressed rats
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Effect of isobaric breathing gas shifts from air to heliox mixtures on resolution of air bubbles in lipid and aqueous tissues of recompressed rats

机译：等压呼吸气体从空气转变为氦氧混合气对再压缩大鼠脂质和水性组织中气泡分离的影响

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Deep tissue isobaric counterdiffusion that may cause unwanted bubble formation or transient bubble growth has been referred to in theoretical models and demonstrated by intravascular gas formation in animals, when changing inert breathing gas from nitrogen to helium after hyperbaric air breathing. We visually followed the in vivo resolution of extravascular air bubbles injected at 101 kPa into nitrogen supersaturated rat tissues: adipose, spinal white matter, skeletal muscle or tail tendon. Bubbles were observed during isobaric breathing-gas shifts from air to normoxic (80:20) heliox mixture while at 285 kPa or following immediate recompression to either 285 or 405 kPa, breathing 80:20 and 50:50 heliox mixtures. During the isobaric shifts, some bubbles in adipose tissue grew marginally for 10–30 min, subsequently they shrank and disappeared at a rate similar to or faster than during air breathing. No such bubble growth was observed in spinal white matter, skeletal muscle or tendon. In spinal white matter, an immediate breathing gas shift after the hyperbaric air exposure from air to both (80:20) and (50:50) heliox, coincident with recompression to either 285 or 405 kPa, caused consistent shrinkage of all air bubbles, until they disappeared from view. Deep tissue isobaric counterdiffusion may cause some air bubbles to grow transiently in adipose tissue. The effect is marginal and of no clinical consequence. Bubble disappearance rate is faster with heliox breathing mixtures as compared to air. We see no reason for reservations in the use of heliox breathing during treatment of air-diving-induced decompression sickness.
机译：理论模型中提到了深层等压压异扩散，可能引起有害的气泡形成或短暂的气泡生长，在高压空气呼吸后将惰性呼吸气体从氮气变为氦气时，动物体内的血管内气体形成证明了这一点。我们在视觉上跟踪了以101 kPa注入过饱和氮气的大鼠组织中的血管外气泡的体内分辨率：脂肪，脊髓白质，骨骼肌或尾腱。在等压呼吸中观察到气泡，气体以285kPa的速度从空气变为常氧（80:20）日光混合气，或者在立即重新压缩为285或405kPa之后，呼吸80:20和50:50的日光混合气。在等压转换过程中，脂肪组织中的一些气泡在10-30分钟内略微增长，随后它们收缩并消失，其消失速度与呼吸期间相似或更快。在脊髓白质，骨骼肌或肌腱中未观察到这样的气泡生长。在脊髓白质中，高压空气从空气暴露于（80:20）和（50:50）日光照射后立即呼吸气体转移，同时再压缩至285kPa或405kPa，导致所有气泡持续收缩，直到他们从视野中消失。深层组织等压反扩散可能导致一些气泡在脂肪组织中短暂生长。效果很小，没有临床后果。与空气相比，使用氦氧混合气呼吸混合物的气泡消失速度更快。我们认为，在因空气潜水引起的减压病的治疗过程中，没有必要保留使用氦氧混合气呼吸的理由。

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