Abstract
According to the OECD statistical base for 2014, anti-depressants will, on average, be distributed at a rate of 62 daily doses per 1,000 inhabitants for the 25 countries surveyed (Health at a glance: Europe 2014; OECD Health Statistics; World Health Organization and OECD Health Statistics, 2014). Divers must be concerned. On another hand, divers are potentially exposed to decompression sickness including coagulation inflammation and ischemia, which can result in neurological lesions or even death. The purpose of this study is to assess whether chronic treatment with anti-depressants may represent a contraindication to the practice of an at-risk activity, such as, scuba diving, or even presents a benefit by attenuating the severity of the symptoms. We study for the first time the effect of a 35-day fluoxetine treatment (20 mg/kg) on the occurrence of decompression sickness in laboratory rats (n = 79). Following exposure to the hazardous protocol, there is a significant correlation between the type of treatment and the clinical status of the rats in favor of a better clinical prognosis for the rats treated with fluoxetine with a significantly higher number of No DCS status and a lower number of Severe DCS status in the Flux, compared to Controls. The treatment modifies the rat performances both significantly and favorably during the physical and behavioral tests, just like their biological and biochemical constants. After decompression, rats under treatment display lower sensory-motor deficit and lowers biochemical disorders. From a biological point of view, we conclude fluoxetine should not be seen as a contraindication for diving on the basis of anticipated increased physiological risk.
Highlights
Gas embolism following an at-risk decompression induces disseminated coagulation, systemic inflammation, and ischemia, which can cause neurological disorders or even death.In animals, we have been able to demonstrate (Blatteau et al, 2012, 2015; Vallee et al, 2016) that fluoxetine administered at a high dose before hyperbaric exposure presents a curative interestRisky Sports with Anti-depressants?in the event of the occurrence of decompression sickness
Over the 36 days of treatment, the Flux rats drank more than the control rats (Ctrl) rats in terms of distribution with a lower consumption in the first 5 days and a higher consumption from the 10th day of treatment (Kolmogorov–SmirnovCtrl/Flux, n = 39/40, p < 0.0001) and in terms of average quantity per day (Beverage: Ctrl = 33.1 ± 1.5 mL, Flux = 35.2 ± 3.7 mL; MWCtrl/Flux, n = 39/40, p < 0.0001)
The weights of the rats subjected to the hyperbaric protocol were similar (Weight: Ctrl = 348.3 ± 19.2 g, Flux = 340.1 ± 22.4 g; MWCtrl/Flux, n = 35/36, p = 0.099)
Summary
Gas embolism following an at-risk decompression induces disseminated coagulation, systemic inflammation, and ischemia, which can cause neurological disorders or even death.In animals, we have been able to demonstrate (Blatteau et al, 2012, 2015; Vallee et al, 2016) that fluoxetine administered at a high dose before hyperbaric exposure presents a curative interestRisky Sports with Anti-depressants?in the event of the occurrence of decompression sickness. Fluoxetine administered in a single high dose (50 mg/kg) has anti-inflammatory properties, as is shown by a reduction in the circulating level of inflammatory markers (Branco-De-Almeida et al, 2011; Blatteau et al, 2012, 2015). The inhibition of NMDA (NR2A) channels by fluoxetine limits the glutamatergic excitotoxicity induced by non-apoptotic cell death. This nonvoltage dependent inhibition could be neuroprotective (Szasz et al, 2007). Administration of fluoxetine has the effect of dilating the small cerebral (Ungvari et al, 1999; SanchezOrtiz et al, 2007), and cutaneous (Lin, 1978) arteries as has been demonstrated in the rat
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