Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “DECOMPRESSION SICKNESS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 631 records · Page 35Linked to original sources
PubMed1991

Simulation of the dynamics of decompression sickness bubbles and the generation of new bubbles.

This communication introduces a system of equations for simulating the dynamics of growth and decay of decompression bubbles. The equations are solved by a numerical method and account for gas diffusion, the action of surface tension, tissue N2 washout by blood, and the rate of ascent from depth. The simulations demonstrate how inward diffusion of N2 can generate a persistent gas bubble from a nucleation process or a nucleus (these are provisionally defined as entities that can give rise to a small bubble of a certain size); an explosive positive-feedback loop is set off as the enlarging radius decreases the pressure due to surface tension. Generation of persistent bubbles is most likely during ascent from depth when PN2 inside any gas phase is decreasing rapidly and PN2 outside is still high before appreciable tissue washout has occurred. The "susceptibility" for the generation of a persistent bubble at any time can be defined as the reciprocal of the difference, at that time, between partial pressure of the nitrogen in tissue and in a spherical bubble of the size that is characteristic of the nucleation process or nucleus; susceptibility is less when ascent is slow because PN2 in bubbles stays high while washout removes N2 from the tissue.

Atmospheric Pressure↗
PubMed1993

Spinal decompression sickness: hydrophobic protein and lamellar bodies in spinal tissue.

Four basic studies have addressed the question of why the spinal cord is so vulnerable to decompression injury, with symptoms exceeding those related to the brain by a ratio often quoted as 3:1. Hydrophobic protein (HP) was discovered in sheep spinal tissue at roughly 3 times (3.3:1) the level in brain and several orders of magnitude greater than in skeletal muscle or plasma. Extravascular lamellar bodies (LBs) of largely phospholipid (PL) were also demonstrated in spinal tissue by electron microscopy using a special fixative, the population being 4.1 times that in brain tissue where some LBs were found adjacent to vascular endothelium. Extracts of spinal surfactant (HP+PL) were found to be particularly surface active on the Langmuir trough, with the HP greatly accelerating monolayer equilibration, especially the recruitment of PL to a rapidly expanding air-aqueous interface. The PL/HP surfactant complex was found to render surfaces hydrophobic when they were able to initiate "strings" of bubbles in supersaturated solutions of gases. These results are discussed as favoring the concept of autochthonous bubbles causing spinal decompression injury exacerbated by the large quantities of spinal surfactant present.

1,2-Dipalmitoylphosphatidylcholine↗