Scientific papers 2011 - 2013
Authors:
Jean-Eric Blatteau, Julien Hugon, Olivier Castagna, Cédric
Meckler, Nicolas Vallée, Yves Jammes, Michel Hugon, Jan
Risberg, and Christophe Pény.
Abstract:
Recent advances in submarine rescue systems have
allowed a transfer under pressure of crew members
rescued from a disabled submarine. The choice of a safe
decompression procedure for pressurized rescuees has
been previously discussed, but no schedule has been
validated when the internal submarine pressure is
significantly increased, i.e., exceeding 2.8 bar absolute
pressure. This study tested a saturation decompression
procedure from hyperbaric exposures up to 6 bar, the
maximum operating pressure of the NATO submarine
rescue system. The objective was to investigate the
incidence of decompression sickness (DCS) and clinical
and spirometric indices of pulmonary oxygen toxicity.
Authors:
Jasna Marinovic, Marko Ljubkovic, Toni Breskovic, Grgo
Gunjaca, Ante Obad, Darko Modun, Nada Bilopavlovic,
Dimitrios Tsikas, Zeljko Dujic.
The aim of this study was to evaluate the changes in
vascular/endothelial function following SCUBA diving and
to assess the potential difference between two breathing
gases: air and nitrox 36 (36% oxygen and 64% nitrogen).
Ten divers performed two 3-day diving series (no-
decompression dive to 18 m with 47 min bottom time
with air and nitrox, respectively), with 2 weeks pause in
between. Arterial/endothelial function was assessed using
SphygmoCor and X ow-mediated dilation measurements,
and the concentration of nitrite before and after diving
was determined in venous blood. Production of nitrogen
bubbles post-dive was assessed by ultrasonic
determination of venous gas bubble grade.
Authors:
Nicolas Vallee, Cédric Meckler, Jean-Jacques Risso, and
Jean-Eric Blatteau.
Nitrogen supersaturation and bubble formation can occur
in the vascular system after diving, leading to death and
nervous disorders from decompression sickness (DCS).
Bubbles alter the vascular endothelium, activate platelets,
and lead to focal ischemia with neurological damage
mediated by the mechanosensitive TREK-1 neuronal
potassium ion channel that sets pre-and postsynaptic
resting membrane potentials. The authors report a
neuroprotective effect associated with TREK-1.
Mice were subjected to decompression from a simulated
90 msw dive. Of 143 mice that were wild type (WT) for
TREK-1, 51.7% showed no DCS, 27.3% failed a grip test,
and 21.0% died. Of 88 TREK-1 knockouts (KO), 26.1%
showed no DCS, 42.0% failed a grip test, and 31.8% died.
Mice that did not express TREK-1 had lower DCS
resistance and were more likely to develop neurological
symptoms. We conclude that the TREK-1 potassium
channel was neuroprotective for DCS.
Authors:
Jean-Eric Blatteau, Sandrine Barre, Aurelie Pascual, Olivier
Castagna, Jacques H. Abraini, Jean-Jacques Risso, &
Nicolas Vallee.
Massive bubble formation after diving can lead to
decompression sickness (DCS) that can result in central
nervous system disorders or even death. Bubbles alter the
vascular endothelium and activate blood cells and
inflammatory pathways, leading to a systemic
pathophysiological process that promotes ischemic
damage. Fluoxetine, a well-known antidepressant, is
recognized as having anti-inflammatory properties at the
systemic level, as well as in the setting of cerebral
ischemia. The authors report a beneficial clinical effect
associated with fluoxetine in experimental DCS. Ninety-
one mice were subjected to a simulated dive at 90 msw
for 45 min before rapid decompression.
Authors:
Stephen R. Thom, Tatyana N. Milovanova, Marina Bogush,
Ming Yang, Veena M. Bhopale, Neal W. Pollock, Marko
Ljubkovic, Petar Denoble, Dennis Madden, Mislav Lozo,
and Zeljko Dujic.
The study goal was to evaluate responses in humans
following decompression from open-water SCUBA diving
with the hypothesis that exertion underwater and use of a
breathing mixture containing more oxygen and less
nitrogen (enriched air nitrox) would alter annexin V-
positive microparticle (MP) production and size changes
and neutrophil activation, as well as their relationships to
intravascular bubble formation.
The documents are classified chronologically from 2011 to 2013.
Click on their descriptions to open and download them.
Authors:
Sema Yilmaz, Kenan Daglioglu, Dincer Yildizdas, Ibrahim
Bayram, Derya Gumurdulu, Sait Polat
Current treatment modalities and new therapeutic
approaches in acute repiratory distress syndrome primarily
focused on the resolution of alveolar edema. These
treatments include glucocorticoids, surfactants, inhaled
nitric oxide, antioxidants and various anti-inflammatory
treatments. Unfortunately, to date, none of these
pharmacologic treatments has proven to be effective. The
authors hypothesized that helium gas might have a
beneficial role in the treatment of ARDS.
Authors: Barbara E. Shykoff & Dan E. Warkander
Combined effects on respiratory minute ventilation (VE )
and, thus, on end-tidal carbon dioxide partial pressure of
breathing resistance and elevated inspired carbon dioxide
had not been determined during heavy exercise. In this
Institutional Review Board-approved, dry, sea-level study,
12 subjects in each of three phases exercised to
exhaustion at 85% peak oxygen uptake while VE and P ET
CO2 were measured. Participants inhaled 0%, 1%, 2%, or
3% CO2 in air, or 0% or 2% CO2 in oxygen, with or
without breathing resistance, mimicking the U.S. Navy’s
MK 16 rebreather underwater breathing apparatus (UBA).
Authors:
Andrea Cortegiani, Grazia Foresta, Giustino Strano, Maria
Teresa Strano, Francesca Montalto, Domenico Garbo,
and Santi Maurizio Raineri
Some cases of decompression illness are known to have
occurred among breath-hold (BH) divers also, and they
are reported in the medical literature. A male BH diver (57
years old), underwater fishing champion, presented
neurological disorders as dizziness, sensory numbness,
blurred vision, and left frontoparietal pain after many
dives to a 30–35 meters sea water depth with short
surface intervals.