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O Hyldegaard

Publications and source records attributed to O Hyldegaard.

7 recordsLinked to original sources

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

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.

Adipose Tissue↗

Effect of SF6-O2 (80/20) breathing on air bubbles in rat tissues.

We studied the effect of SF6-O2 breathing on air bubbles injected into skeletal muscle, rat-tail tendon, the anterior chamber of the eye, and spinal white matter. Decompression-induced nitrogen bubbles in adipose tissue were studied during breathing of SF6-O2 (80/20). The results of SF6-O2 breathing are compared with previous experiments using heliox (80/20) as the breathing medium. Bubbles studied in skeletal muscle, eye chamber, and spinal white matter were found to behave in a two-phased manner during SF6-O2 (80/20) breathing. All bubbles would initially decrease rapidly in size for a period of 10-80 min (depending on the tissue). Subsequently, the bubbles stabilized and decreased in size with a shrinking rate near zero. In spinal white matter, very small bubbles decreased size with a shrinking rate near zero. In spinal white matter, very small bubbles could disappear before development of the slow phase. All bubbles in tendon shrank at a rather constant rate during SF6-O2 (80/20) breathing until they disappeared. During SF6-O2 (80/20) breathing, all bubbles in adipose tissue shrank and disappeared at least as fast as during heliox (80/20) breathing. Just before disappearance of the bubbles the shrinking rate slowed. Comparison of the effects of SF6-O2 (80/20) and heliox (80/20) breathing suggests that countercurrent gas exchange is at work in some tissues.

Adipose Tissue↗

Diving physiology and pathophysiology.

Divers have worked at 500 m depth in the sea and have reached 700 m in simulated chamber dives. A prerequisite for this has been extensive physiological studies of the body's reactions to pressure and pressure changes. This paper reviews such physiological and pathophysiological studies with emphasis on recent developments.

Decompression Sickness↗

Effect of air, heliox, and oxygen breathing on air bubbles in aqueous tissues in the rat.

Our purpose was to examine the behavior of air bubbles in three non-lipid tissues (skeletal muscle, tendon, and the anterior chamber of the eye) during breathing of air, helium-oxygen (heliox, 80:20), or oxygen. Air bubbles were injected into skeletal muscle or tendon in rats after decompression from a 1-h air exposure at 3.5 atm abs (355 kPa) or into the anterior chamber of the rat eye without any previous pressure exposure. The bubbles were studied by photomicroscopy at 1 atm abs (101 kPa) during either air breathing or during air breathing followed by heliox or O2 breathing. Muscle: during air breathing, all bubbles initially increased in size for a period of 55-100 min after decompression and then started to shrink. Both heliox and O2 breathing increased the shrinking rate as compared to air. Bubble size decreased more rapidly during O2 than heliox breathing. Tendon: during air breathing, bubble size decreased at a constant rate; in one bubble the decrease was preceded by a small increase. During heliox breathing most bubbles decreased faster than during breathing of air. O2 breathing caused a short-term increase in bubble size in 4 out of 10 bubbles. Otherwise, the shrinkage rate was increased in six bubbles and uninfluenced in four bubbles during breathing of O2. Rat eye: during air breathing all bubbles shrank in the observation period. When heliox breathing was started, all bubbles transiently grew for 10-35 min, after which they began shrinking faster than during air breathing. When O2 breathing was started, five out of seven bubbles initially grew or stopped shrinking for 5-15 min, after which they decreased in size faster than during both air and heliox breathing. We conclude that breathing of either heliox or O2 will cause air bubbles in aqueous tissues to disappear faster than during breathing of air. Since heliox breathing promoted bubble shrinking in both muscle and tendon, gas exchange was probably not primarily limited by extravascular diffusion in these aqueous tissues. The present experiments suggest that heliox breathing at 1 atm abs may not exacerbate limb bends.

Air↗

Protective effect of oxygen and heliox breathing during development of spinal decompression sickness.

A rat model of spinal decompression sickness (DCS) allows study of spinal cord function for at least 3 h after decompression to 1 atm abs (101 kPa) after an exposure to air at 3.8 atm abs (385 kPa) for 1 h. During these 3 h, spinal evoked potentials (SEPs) elicited by peroneal nerve stimulation may be reduced or disappear, and histologic lesions in the spinal cord are observed. Three groups of animals were given either air, oxygen, or heliox (80/20) to breathe at 1 atm abs for 3 h after decompression. Both oxygen and heliox breathing impeded the development of DCS significantly as judged by the mortality of the animals and disappearance of the SEPs. The effect of heliox seemed to be superior to that of oxygen. The latency time from stimulation to the first SEP peak increased significantly during both air and oxygen breathing, whereas no significant increase was seen during heliox breathing. Histologic examination of the spinal cords of animals breathing air, oxygen, or heliox (80/20) showed focal lesions in the white and gray matter. In the white matter, degenerated myelin sheaths as well as expanded extracellular spaces compatible with bubble formation were seen. In the gray matter, perikaryal degeneration was observed. The extracellular space in the white matter was increased in all decompressed animals compared with controls (P < 0.01). Oxygen and heliox breathing caused a smaller increase in extracellular space as compared with air-breathing animals (P < 0.05) and (0.10 > P > 0.05), respectively. It is concluded that breathing of oxygen or heliox (80/20) at 1 atm abs has a preventive effect on the development of DCS when compared with air breathing; the effect of heliox seems to be superior to that of oxygen.

Air↗

Influence of heliox, oxygen, and N2O-O2 breathing on N2 bubbles in adipose tissue.

Bubbles in rat adipose tissue were studied at 1 bar after decompression from an exposure to air at 3.3 bars (absolute) for 4 h. During air breathing the bubbles grew throughout the observation period. During heliox (80:20) breathing they shrank and eventually disappeared from view. If the breathing gas was changed from heliox back to air or to N2O-O2 (80:20) while the bubbles still had an appreciable size, they started growing again. If the change to N2O was done after or a few minutes before a bubble disappeared from view, it did not reappear. During breathing of 100% O2, most bubbles containing N2 initially grew and then maintained their size for a while before diminishing. However, some bubbles did not start shrinking during the 2-3-h observation period. The relevance of the findings to heliox treatment of CNS decompression sickness after air dives is discussed.

Adipose Tissue↗

Effect of He-O2, O2, and N2O-O2 breathing on injected bubbles in spinal white matter.

Injected air bubbles in spinal white matter in the rat were studied at 1 bar after decompression from an exposure to air at 3.1 bar (absolute) for 4 h. During air breathing all injected bubbles grew for the first 2 h of the observation period. Thereafter three of nine bubbles began to shrink and one of them disappeared. During breathing of heliox (80:20) bubbles consistently shrank and disappeared from view. If the breathing gas was changed from heliox to N2O-O2 (80:20), while bubbles still had an appreciable size, they started growing again. If the change to N2O-O2 was done after a bubble disappeared from view, it did not reappear. During breathing of 100% oxygen, all bubbles initially grew. Subsequently they all shrank and disappeared at about the same time after gas shift, as during heliox breathing. The effect of heliox treatment on CNS decompression sickness after air dives is discussed.

Adipose Tissue↗