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. We report a beneficial clinical effect associated with
fluoxetine in experimental DCS. 91 mice were subjected to a simulated dive at 90 msw for 45 min before rapid
decompression. The experimental group received 50 mg/kg of
fluoxetine 18 hours before hyperbaric exposure (n = 46) while controls were not treated (n = 45). Clinical assessment took place over a period of 30 min after surfacing. At the end, blood samples were collected for blood cells counts and
cytokine IL-6 detection. There were significantly fewer manifestations of DCS in the
fluoxetine group than in the controls (43.5% versus 75.5%, respectively; p = 0.004). Survivors showed a better and significant neurological recovery with
fluoxetine. Platelets and red cells were significantly decreased after
decompression in controls but not in the treated mice.
Fluoxetine reduced circulating
IL-6, a relevant marker of systemic
inflammation in DCS. We concluded that
fluoxetine decreased the incidence of DCS and improved motor recovery, by limiting
inflammation processes.