Background: Immersion can cause immersion pulmonary edema (IPE) in previously healthy subjects. We performed a case-control study to better identify IPE risk factors.
Methods: We prospectively included recreational scuba divers who had presented signs of IPE and control divers who were randomly chosen among diving members of the French Underwater Federation.
Despite state-of-the-art hyperbaric oxygen (HBO) treatment, about 30% of patients suffering neurologic decompression sickness (DCS) exhibit incomplete recovery. Since the mechanisms of neurologic DCS involve ischemic processes which result in excitotoxicity, it is likely that HBO in combination with an anti-excitotoxic treatment would improve the outcome in patients being treated for DCS. Therefore, in the present study, we investigated the effect of the noble gas xenon in an ex vivo model of neurologic DCS.
View Article and Find Full Text PDFBackground: Current in vivo methods cannot distinguish between the roles of vascular and stationary tissular gas bubbles in the mechanisms of decompression sickness (DCS).
New Method: To answer this question, we designed a normobaric-hyperbaric chamber for studying specifically the contribution of stationary tissular gas bubbles in the mechanisms of DCS in individually-superfused tissue samples. For validating our method, we investigated in rat brain slices exposed to 0.
Immersion pulmonary edema in scuba divers is a rare disorder that tends to recur and can be potentially fatal, even in the absence of underlying cardiac disease. Anecdotal cases of reversible myocardial dysfunction have been described in this setting, but little is known of its pathogenesis. The purpose of the present study was to determine the clinical outcomes and the determinants associated with this condition.
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