Despite "gold standard" hyperbaric oxygen treatment, 30% of patients suffering from neurological decompression sickness still exhibit incomplete recovery, including sensory impairments. Fluoxetine, a well-known antidepressant, is recognized as having anti-inflammatory effects in the setting of cerebral ischemia. In this study, we focused on the assessment of sensory neurological deficits and measurement of circulating cytokines after decompression in rats treated or not with fluoxetine. 78 rats were divided into a clinical (n=38) and a cytokine (n=40) group. In both groups, the rats were treated with fluoxetine (30mg/kg PO, 6 h beforehand) or with a saccharine solution. All the rats were exposed to 90 msw for 45 min before staged decompression. In the clinical group, Paw Withdrawal Force (PWF) after mechanical stimulation and Paw Withdrawal Latency (PWL) after thermal stimulation were evaluated before, 1 h and 48 h after surfacing. At 48 h a dynamic weight-bearing (DWB) device was used to assess postural stability depending on the time spent on 3 or 4 paws. For cytokine analysis, blood samples were collected from the vena cava 1 h after surfacing. PWF and PWL were increased after surfacing in the controls but not in the fluoxetine group. DWB assessment highlighted a better stability on 3 paws for the fluoxetine group. IL10 levels were significantly decreased after decompression in the controls but maintained at baseline level with fluoxetine. This study suggests that Fluoxetine has a beneficial effect on sensory neurological recovery. We hypothesize that the observed effect is mediated through maintained anti-inflammatory cytokine IL10 production.
- decompression sickness
- Copyright © 2015, Journal of Applied Physiology