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. Seventy-eight rats were divided into a clinical (n = 38) and a
cytokine (n = 40) group. In both groups, the rats were treated with
fluoxetine (30 mg/kg po, 6 h beforehand) or with a saccharine
solution. All of the rats were exposed to 90 m seawater for 45 min before staged
decompression. In the clinical group, paw withdrawal force after mechanical stimulation and paw withdrawal latency after thermal stimulation were evaluated before and 1 and 48 h after surfacing. At 48 h, a dynamic weight-bearing device was used to assess postural stability, depending on the time spent on three or four paws. For
cytokine analysis, blood samples were collected from the vena cava 1 h after surfacing. Paw withdrawal force and latency were increased after surfacing in the controls, but not in the
fluoxetine group. Dynamic weight-bearing assessment highlighted a better stability on three paws for the
fluoxetine group.
IL-10 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 IL-10 production.