Effect of hypobaric air, oxygen, heliox (50:50), or heliox (80:20) breathing on air bubbles in adipose tissue

The fate of bubbles formed in tissues during decompression to altitude after diving or due to accidental loss of cabin pressure during flight has only been indirectly inferred from theoretical modeling and clinical observations with noninvasive bubble-measuring techniques of intravascular bubbles. In this report we visually followed the in vivo resolution of micro-air bubbles injected into adipose tissue of anesthetized rats decompressed from 101.3 kPa to and held at 71 kPa corresponding to ∼2.750 m above sea level, while the rats breathed air, oxygen, heliox (50:50), or heliox (80:20). During air breathing, bubbles initially grew for 30–80 min, after which they remained stable or began to shrink slowly. Oxygen breathing caused an initial growth of all bubbles for 15–85 min, after which they shrank until they disappeared from view. Bubble growth was significantly greater during breathing of oxygen compared with air and heliox breathing mixtures. During heliox (50:50) breathing, bubbles initially grew for 5–30 min, from which point they shrank until they disappeared from view. After a shift to heliox (80:20) breathing, some bubbles grew slightly for 20–30 min, then shrank until they disappeared from view. Bubble disappearance was significantly faster during breathing of oxygen and heliox mixtures compared with air. In conclusion, the present results show that oxygen breathing at 71 kPa promotes bubble growth in lipid tissue, and it is possible that breathing of heliox may be beneficial in treating decompression sickness during flight.

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Effect of oxygen and heliox breathing on air bubbles in adipose tissue during 25-kPa altitude exposures

Journal of Applied Physiology ◽

10.1152/japplphysiol.90840.2008 ◽

2008 ◽

Vol 105 (5) ◽

pp. 1492-1497 ◽

Cited By ~ 3

Author(s):

T. Randsøe ◽

T. M. Kvist ◽

O. Hyldegaard

Keyword(s):

Adipose Tissue ◽

Bubble Growth ◽

Decompression Sickness ◽

Nitrogen Pressure ◽

Growth Time ◽

Air Bubbles ◽

Oxygen Breathing ◽

Effect Of Oxygen ◽

Tissue Nitrogen

At altitude, bubbles are known to form and grow in blood and tissues causing altitude decompression sickness. Previous reports indicate that treatment of decompression sickness by means of oxygen breathing at altitude may cause unwanted bubble growth. In this report we visually followed the in vivo changes of micro air bubbles injected into adipose tissue of anesthetized rats at 101.3 kPa (sea level) after which they were decompressed from 101.3 kPa to and held at 25 kPa (10,350 m), during breathing of oxygen or a heliox(34:66) mixture (34% helium and 66% oxygen). Furthermore, bubbles were studied during oxygen breathing preceded by a 3-h period of preoxygenation to eliminate tissue nitrogen before decompression. During oxygen breathing, bubbles grew from 11 to 198 min (mean: 121 min, ±SD 53.4) after which they remained stable or began to shrink slowly. During heliox breathing bubbles grew from 30 to 130 min (mean: 67 min, ±SD 31.0) from which point they stabilized or shrank slowly. No bubbles disappeared during either oxygen or heliox breathing. Preoxygenation followed by continuous oxygen breathing at altitude caused most bubbles to grow from 19 to 179 min (mean: 51 min, ±SD 47.7) after which they started shrinking or remained stable throughout the observation period. Bubble growth time was significantly longer during oxygen breathing compared with heliox breathing and preoxygenated animals. Significantly more bubbles disappeared in preoxygenated animals compared with oxygen and heliox breathing. Preoxygenation enhanced bubble disappearance compared with oxygen and heliox breathing but did not prevent bubble growth. The results indicate that oxygen breathing at 25 kPa promotes air bubble growth in adipose tissue regardless of the tissue nitrogen pressure.

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Effect of combined recompression and air, oxygen, or heliox breathing on air bubbles in rat tissues

Journal of Applied Physiology ◽

10.1152/jappl.2001.90.5.1639 ◽

2001 ◽

Vol 90 (5) ◽

pp. 1639-1647 ◽

Cited By ~ 10

Author(s):

O. Hyldegaard ◽

D. Kerem ◽

Y. Melamed

Keyword(s):

Adipose Tissue ◽

White Matter ◽

Decompression Sickness ◽

Rat Tissues ◽

Air Bubbles ◽

Transient Growth ◽

Air Exposure ◽

Air Breathing ◽

Oxygen Breathing ◽

Clinical Observations

The fate of bubbles formed in tissues during the ascent from a real or simulated air dive and subjected to therapeutic recompression has only been indirectly inferred from theoretical modeling and clinical observations. We visually followed the resolution of micro air bubbles injected into adipose tissue, spinal white matter, muscle, and tendon of anesthetized rats recompressed to and held at 284 kPa while rats breathed air, oxygen, heliox 80:20, or heliox 50:50. The rats underwent a prolonged hyperbaric air exposure before bubble injection and recompression. In all tissues, bubbles disappeared faster during breathing of oxygen or heliox mixtures than during air breathing. In some of the experiments, oxygen breathing caused a transient growth of the bubbles. In spinal white matter, heliox 50:50 or oxygen breathing resulted in significantly faster bubble resolution than did heliox 80:20 breathing. In conclusion, air bubbles in lipid and aqueous tissues shrink and disappear faster during recompression during breathing of heliox mixtures or oxygen compared with air breathing. The clinical implication of these findings might be that heliox 50:50 is the mixture of choice for the treatment of decompression sickness.

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Effect of oxygen breathing and perfluorocarbon emulsion treatment on air bubbles in adipose tissue during decompression sickness

Journal of Applied Physiology ◽

10.1152/japplphysiol.00785.2009 ◽

2009 ◽

Vol 107 (6) ◽

pp. 1857-1863 ◽

Cited By ~ 10

Author(s):

T. Randsoe ◽

O. Hyldegaard

Keyword(s):

Adipose Tissue ◽

Bubble Growth ◽

Decompression Sickness ◽

Combined Effect ◽

Inert Gases ◽

Air Bubbles ◽

Transport Capacity ◽

Normobaric Oxygen ◽

Oxygen Breathing ◽

Effect Of Oxygen

Decompression sickness (DCS) after air diving has been treated with success by means of combined normobaric oxygen breathing and intravascular perfluorocarbon (PFC) emulsions causing increased survival rate and faster bubble clearance from the intravascular compartment. The beneficial PFC effect has been explained by the increased transport capacity of oxygen and inert gases in blood. However, previous reports have shown that extravascular bubbles in lipid tissue of rats suffering from DCS will initially grow during oxygen breathing at normobaric conditions. We hypothesize that the combined effect of normobaric oxygen breathing and intravascular PFC infusion could lead to either enhanced extravascular bubble growth on decompression due to the increased oxygen supply, or that PFC infusion could lead to faster bubble elimination due to the increased solubility and transport capacity in blood for nitrogen causing faster nitrogen tissue desaturation. In anesthetized rats decompressed from a 60-min hyperbaric exposure breathing air at 385 kPa, we visually followed the resolution of micro-air bubbles injected into abdominal adipose tissue while the rats breathed either air, oxygen, or oxygen breathing combined with PFC infusion. All bubble observations were done at 101.3 kPa pressure. During oxygen breathing with or without combined PFC infusion, bubbles disappeared faster compared with air breathing. Combined oxygen breathing and PFC infusion caused faster bubble disappearance compared with oxygen breathing. The combined effect of oxygen breathing and PFC infusion neither prevented nor increased transient bubble growth time, rate, or growth ratio compared with oxygen breathing alone. We conclude that oxygen breathing in combination with PFC infusion causes faster bubble disappearance and does not exacerbate transient bubble growth. PFC infusion may be a valuable adjunct therapy during the first-aid treatment of DCS at normobaric conditions.

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Effect of oxygen breathing on micro oxygen bubbles in nitrogen-depleted rat adipose tissue at sea level and 25 kPa altitude exposures

Journal of Applied Physiology ◽

10.1152/japplphysiol.00193.2012 ◽

2012 ◽

Vol 113 (3) ◽

pp. 426-433 ◽

Cited By ~ 1

Author(s):

Thomas Randsoe ◽

Ole Hyldegaard

Keyword(s):

Adipose Tissue ◽

Sea Level ◽

Kinetic Models ◽

Bubble Growth ◽

Decompression Sickness ◽

Ambient Pressure ◽

Bubble Formation ◽

Nitrogen Pressure ◽

Oxygen Breathing ◽

Effect Of Oxygen

The standard treatment of altitude decompression sickness (aDCS) caused by nitrogen bubble formation is oxygen breathing and recompression. However, micro air bubbles (containing 79% nitrogen), injected into adipose tissue, grow and stabilize at 25 kPa regardless of continued oxygen breathing and the tissue nitrogen pressure. To quantify the contribution of oxygen to bubble growth at altitude, micro oxygen bubbles (containing 0% nitrogen) were injected into the adipose tissue of rats depleted from nitrogen by means of preoxygenation (fraction of inspired oxygen = 1.0; 100%) and the bubbles studied at 101.3 kPa (sea level) or at 25 kPa altitude exposures during continued oxygen breathing. In keeping with previous observations and bubble kinetic models, we hypothesize that oxygen breathing may contribute to oxygen bubble growth at altitude. Anesthetized rats were exposed to 3 h of oxygen prebreathing at 101.3 kPa (sea level). Micro oxygen bubbles of 500-800 nl were then injected into the exposed abdominal adipose tissue. The oxygen bubbles were studied for up to 3.5 h during continued oxygen breathing at either 101.3 or 25 kPa ambient pressures. At 101.3 kPa, all bubbles shrank consistently until they disappeared from view at a net disappearance rate (0.02 mm2 × min−1) significantly faster than for similar bubbles at 25 kPa altitude (0.01 mm2 × min−1). At 25 kPa, most bubbles initially grew for 2–40 min, after which they shrank and disappeared. Four bubbles did not disappear while at 25 kPa. The results support bubble kinetic models based on Fick's first law of diffusion, Boyles law, and the oxygen window effect, predicting that oxygen contributes more to bubble volume and growth during hypobaric conditions. As the effect of oxygen increases, the lower the ambient pressure. The results indicate that recompression is instrumental in the treatment of aDCS.

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Effect of oxygen breathing and perfluorocarbon emulsion treatment on air bubbles in adipose tissue during decompression sickness

Yearbook of Sports Medicine ◽

10.1016/s0162-0908(10)79643-4 ◽

2010 ◽

Vol 2010 ◽

pp. 314-315

Author(s):

R.J. Shephard

Keyword(s):

Adipose Tissue ◽

Decompression Sickness ◽

Air Bubbles ◽

Perfluorocarbon Emulsion ◽

Oxygen Breathing ◽

Effect Of Oxygen

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ACQUIRED STORAGE POOL DISEASE IN DECOMPRESSION SICKNESS

10.1055/s-0038-1644563 ◽

1987 ◽

Author(s):

H Yamazaki ◽

K Tanoue ◽

K Kuroiwa ◽

H Suzuki ◽

M Shibayama ◽

...

Keyword(s):

Time Course ◽

Decompression Sickness ◽

Adenine Nucleotide ◽

Regression Line ◽

Kinetic Studies ◽

Air Bubbles ◽

Platelet Counts ◽

Storage Pool ◽

Storage Pool Disease

The presence of hemostatic abnormalities has been reported in decompression sickness. It is suggested that platelets recognize air bubbles in the blood stream as a foreign surface and adhere to them with ensuing platelet aggregation. It is important to determine if consumption of platelets occurs in vivo to understand a role of platelets in the genesis of decompression sickness. To analyse the problem, platelet behavior was studied in 34 rabbits with decompression sickness which was brought about by the exposure to 6 ATA (atmospheres absolute) for 40 min followed by rapid decompression. All rabbits died within one hr after the decompression due to apnea which always preceded the cardiac arrest. Platelet counts decreased significantly during the time course of decompression. A regression line can be drawn between the changes in platelet count (Y) and the time after decompression (X): Y=100.2 - 0.8X, r= -0.876, p<0.001. Platelet counts measured just before the apnea were 56 to 72% (65.7 ± 6.1%) of the precompression value. Kinetic studies with 111 In-oxine-labeled platelets revealed shortened survivals of the circulating platelets and autoradiograms indicated the accumulation of radioactivity in the lungs after the decompression. Although there was no change in the mode volume of platelets after the decompression, the transient appearance of smaller or fragmented platelets suggested a random over-destruction of platelets. Whole and releasable adenine nucleotide contents of platelets decreased significantly after the decompression. There were no significant changes in cytoplasmic adenine nucleotide contents. Therefore, in decompression sickness, the circulating platelets behaved similarly to those of acquired storage pool disease. Platelet thrombi were found in the pulmonary artery, compatible with the accumulation of the labeled platelets. These findings suggest that circulating air-bubbles interact with circulating platelets, causing the platelet release reaction, and these activated platelets participate in the formation of thrombi in decompression sickness.

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Functional characterization of human brown adipose tissue metabolism

Biochemical Journal ◽

10.1042/bcj20190464 ◽

2020 ◽

Vol 477 (7) ◽

pp. 1261-1286 ◽

Cited By ~ 3

Author(s):

Marie Anne Richard ◽

Hannah Pallubinsky ◽

Denis P. Blondin

Keyword(s):

Adipose Tissue ◽

Brown Adipose Tissue ◽

Functional Characterization ◽

Human Infants ◽

Positron Emission ◽

Brown Adipose ◽

Treatment Of Obesity ◽

And Function

Brown adipose tissue (BAT) has long been described according to its histological features as a multilocular, lipid-containing tissue, light brown in color, that is also responsive to the cold and found especially in hibernating mammals and human infants. Its presence in both hibernators and human infants, combined with its function as a heat-generating organ, raised many questions about its role in humans. Early characterizations of the tissue in humans focused on its progressive atrophy with age and its apparent importance for cold-exposed workers. However, the use of positron emission tomography (PET) with the glucose tracer [18F]fluorodeoxyglucose ([18F]FDG) made it possible to begin characterizing the possible function of BAT in adult humans, and whether it could play a role in the prevention or treatment of obesity and type 2 diabetes (T2D). This review focuses on the in vivo functional characterization of human BAT, the methodological approaches applied to examine these features and addresses critical gaps that remain in moving the field forward. Specifically, we describe the anatomical and biomolecular features of human BAT, the modalities and applications of non-invasive tools such as PET and magnetic resonance imaging coupled with spectroscopy (MRI/MRS) to study BAT morphology and function in vivo, and finally describe the functional characteristics of human BAT that have only been possible through the development and application of such tools.

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