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Biomedical subjects

E A Hemmingsen

Publications and source records attributed to E A Hemmingsen.

At least 19 recordsLinked to original sources
PubMed1990

Gas supersaturation tolerances in amoeboid cells before and after ingestion of bubble-promoting particles.

Macrophages and other cells are capable of ingesting a variety of solids from their external environment. When such phagocytic processes occur in animals, they can lead to phagocytosis from the respiratory or the digestive tract of particles containing minute air emobli that may serve as bubble nuclei upon exposure of the animal to conditions of gas supersaturation. To test whether this is possible, gas supersaturation tolerances were determined for murine macrophages and macrophage-like tumor cells, and for cells of the slime mold Dictyostelium discoideum, before and after phagocytosis of particles that were effective in inducing bubble formation in nitrogen-supersaturated aqueous suspensions. After phagocytosis, the ability of the particles to induce bubble formation was completely abolished. All three cell types essentially retained their normal high resistance to bubble formation; even nitrogen supersaturations in excess of 150 atm (1.55 x 10(7) Pa) did not lead to internal bubbles. Alterations of the particle surfaces and unique properties of the intracellular fluid appear to be the underlying cause of the extremely high gas supersaturation tolerances observed.

Animals↗
PubMed1990

Bubble formation properties of hydrophobic particles in water and cells of Tetrahymena.

It is generally assumed that hydrophobic surfaces play a role in bubble formation in vivo, but no tests of this assumption seem to exist. Model systems for both in vitro and in vivo study of the bubble nucleation properties of hydrophobic surfaces were developed. First, aqueous suspensions of particles were exposed to gas supersaturations, and the numbers of bubbles that formed were determined. Although the supersaturation thresholds for spontaneous bubble nucleation in pure water exceeds 175 atmospheres gas tension, gas tensions of only a few atmospheres caused the profuse formation of bubbles with the most effective particles. Some or most of this latter effect seemed to be caused by gas trapped in irregularities on the particles. Second, particles that were especially effective bubble promoters were added to suspensions of ciliates. Upon their ingestion, all of the particles lost their ability to induce bubble formation in the cells with supersaturations equal to or exceeding the threshold for spontaneous nucleation in water. These results indicate that intracellular bubble formation may not occur readily in vivo.

Animals↗
PubMed1987

Lack of bubble formation in hypobarically decompressed cells.

Suspensions of human erythrocytes or of unicellular microorganisms (Tetrahymena pyriformis, Euglena gracilis, Escherichia coli, and Microcyclus aquaticus) were equilibrated with nitrogen gas pressures up to 200 atm and rapidly decompressed to hypobaric pressures below the vapor point of water. The intracellular environments proved to be very tolerant to the gas supersaturations induced. None or only a few cells were damaged in each case, and bubbles were never observed intracellularly after decompression. In view of such extreme tolerances, it is doubtful that bubbles originate intracellularly during decompression of multicellular organisms, in which bubbles occur with far lower gas supersaturations, unless the tolerances are greatly affected by extensive mechanical deformations of the cells or by the presence of internalized particles with bubble-promoting properties.

Animals↗
PubMed1985

Swimming movements initiate bubble formation in fish decompressed from elevated gas pressures.

Young specimens of trout, catfish, sculpin and salamanders were equilibrated with elevated gas pressures, then rapidly decompressed to ambient pressure. The newly hatched forms tolerated extremely high gas supersaturations; equilibration pressures of 80-120 atm argon or 150-250 atm helium were required for in vivo bubble formation. During subsequent larval development, the equilibration pressures required decreased to just 5-10 atm and bubbles originated in the fins. Anesthetising older fish before decompression prevented bubble formation in the fins; this suggests that swimming movements mechanically initiate bubbles, possibly by a tribonucleation mechanism.

Ambystoma↗
PubMed1985

Intracellular gas supersaturation tolerances of erythrocytes and resealed ghosts.

Intact mammalian, avian, and amphibian erythrocytes were saturated with up to 300 atm nitrogen or argon gas and rapidly decompressed. Despite the profuse nucleation of gas bubbles in the suspending fluid, no evidence of intracellular gas bubble nucleation was found; all or most of the cells remained intact and little or no hemoglobin escaped. Internal bubbles were similarly absent from resealed ghosts of human erythrocytes as shown by lack of disintegration and by retention of an entrapped fluorescent compound. The absence of bubbles may indicate that much of the internal water does not have the same nucleation properties as external water.

Animals↗
PubMed1985

A direct test for the survival of gaseous nuclei in vivo.

It has recently been demonstrated that bubble formation in the crab Pachygrapsus crassipes is induced by limb motions following decompression from nitrogen pressures as low as 2 atm. Preformed gaseous nuclei are not involved in this process and are absent from this animal. We further demonstrate here that nuclei do not remain in the body fluids when the motion-induced bubbles dissolve. This shows that gas phases do not become protected against dissolution in vivo as has been proposed by other workers. This may have important implications concerning the origin of bubbles causing decompression sickness in higher animals.

Aerospace Medicine↗
PubMed1984

Bubble formation in crustaceans following decompression from hyperbaric gas exposures.

In vivo bubble formation was studied in various crustaceans equilibrated with high gas pressures and rapidly decompressed to atmospheric pressure. The species varied widely in susceptibility to bubble formation, and adults were generally more susceptible than larval stages. Bubbles did not form in early brine shrimp larvae unless equilibration pressures of at least 175 atm argon or 350 atm helium were used; for adult brine shrimp, copepods, and the larvae of crabs and shrimps, 100-125 atm argon or 175-225 atm helium were required. In contrast, bubbles formed in the leg joints of megalopa and adult crabs following decompression from only 3-10 atm argon; stimulation of limb movements increased this bubble formation, whereas inhibition of movements decreased it. High hydrostatic compressions applied before gas equilibration or slow compressions did not affect bubble formation. We concluded that circulatory systems, musculature, and storage lipids do not necessarily render organisms susceptible to bubble formation and that bubbles do not generally originate as preformed nuclei. In some cases, tribonucleation appears to be the cause of the bubbles.

Animals↗
PubMed1984

Bubble formation in crabs induced by limb motions after decompression.

In vivo bubble formation was studied in the megalopal stage of the crab Pachygrapsus crassipes. The animals were equilibrated with elevated argon, nitrogen, or helium pressures then rapidly decompressed to atmospheric pressure. Voluntary motions induced bubble nucleation in leg joints after exposures to as low as 2 atm nitrogen (gauge pressure). Delays of several minutes sometimes passed between decompression and bubble formation. Mechanically stimulating the animals to move their legs increased this bubble formation, whereas immobilizing the legs before gas equilibration prevented it, even in animals decompressed from 150 atm nitrogen. We conclude that preformed nuclei are not responsible for bubbles developing in the legs of this animal. Instead, tribonucleation of bubbles apparently occurs as a result of limb motions at relatively low gas supersaturations.

Animals↗
PubMed1980

Rupture of the cell envelope by induced intracellular gas phase expansion in gas vacuolate bacteria.

Using a new approach, we estimated the physical strength of the cell envelopes of three species of gram-negative, gas vacuolate bacteria (Microcyclus aquaticus, Prosthecomicrobium pneumaticum, and Meniscus glaucopis). Populations of cells were slowly (0.5 to 2.9 h) saturated with argon, nitrogen, or helium to final pressures up to 100 atm (10, 132 kPa). The gas phases of the vesicles remained intact and, upon rapid (1 to 2 s) decompression to atmospheric pressure, expanded and ruptured the cells; loss of colony-forming units was used as an index of rupture. Because the cell envelope is the cellular component most likely to resist the expanding intracellular gas phase, its strength can be estimated from the minimum gas pressures that produce rupture. The viable counts indicated that these minimum pressures were between 25 and 50 atm; the majority of the cell envelopes were ruptured at pressures between 50 and 100 atm. Cells in which the gas vesicles were collapsed and the gas phases were effectively dissolved by rapid compression tolerated decompression from much higher gas saturations. Cells that do not normally possess gas vesicles (Escherichia coli) or that had been prevented from forming them by addition of L-lysine to the medium (M. aquaticus) were not harmed by decompression from gas saturation pressures up to 300 atm.

Atmospheric Pressure↗
PubMed1979

Lack of intracellular bubble formation in microorganisms at very high gas supersaturations.

Eucaryotic unicellular (a yeast, a cellular slime mold, and various protozoans) and two multicellular (aschelminths) microorganisms were saturated with gas at high pressures and rapidly decompressed. No effect was observed with pressures of argon up to 125 atm, nitrogen up to 175 atm, and helium up to 350 atm, showing that the induced gas supersaturations did not cause intracellular bubbles to form. With 25--50 atm higher gas pressures, the decompression usually produced killing and cell rupture, although differences in tolerances existed among the various organisms. Substantial fractions of the populations survived gas supersaturations well above the threshold values for massive spontaneous nucleation of bubbles in the water. When killing occurred, external rather than internal bubbles appeared to be the cause. Even with the 300 atm argon or nitrogen pressures, yeast cells were unaffected, apparently because of the external protection provided by their cell wall. It is concluded that the gas supersaturations required for intracellular formation of bubbles generally are at least equal to and probably higher than the bubble nucleation thresholds for water or aqueous solutions.

Animals↗
PubMed1977

Spontaneous formation of bubbles in gas-supersaturated water.

Spontaneous nucleation of bubbles may occur in water subjected to heating, tensile stress, or gas-supersaturation. Large discrepancies exist between the threshold nucleation conditions predicted theoretically and those indicated by empirical observations. The theoretical approaches have been hampered by inadequate understanding of many of the submicroscopic and molecular properties of liquids, and experimental obstacles have included the always present and difficult to control interference from pre-existing nuclei. These problems have been most pronounced for nucleation induced by dissolved gas; indeed, nucleation thresholds for any gas/liquid system are unknown due to a lack of relevant empirical data, and no quantitative theories seem to exist.

Argon↗