Protective effects of fluoxetine on decompression sickness in mice

• Published in: PloS one 2012-11, Vol.7 (11), p.e49069-e49069
• Main Authors: Blatteau, Jean-Eric, Barre, Sandrine, Pascual, Aurelie, Castagna, Olivier, Abraini, Jacques H, Risso, Jean-Jacques, Vallee, Nicolas
• Format: Article
• Language: English
• Subjects: Animals; Anti-inflammatory agents; Aviation; Biology; Blood; Blood cells; Blood platelets; Brain research; Central nervous system; Cytokines; Decompression; Decompression sickness; Decompression Sickness - drug therapy; Decompression Sickness - pathology; Diving; Diving - physiology; Drug dosages; Embolism, Air - drug therapy; Embolism, Air - pathology; Embolisms; Endothelium; Endothelium, Vascular - drug effects; Endothelium, Vascular - pathology; Environmental health; Fluoxetine; Fluoxetine - administration & dosage; Humans; Inflammation; Interleukin 6; Ischemia; Laboratories; Medical research; Medicine; Mice; Nervous system diseases; Platelet Count; Platelets; Protective Agents - administration & dosage; Pulmonary arteries; Recovery; Serotonin; Spinal cord; Stroke; Studies; Surfacing
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0049069

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.