Abstract
Vascular bubble formation after decompression contributes to endothelial injuries which form the basis for the development of decompression sickness (DCS). Nitric oxide (NO) is a powerful vasodilator that contributes to vessel homeostasis. It has been shown that NO-releasing agent may reduce bubble formation and prevent serious decompression sickness. The use of sildenafil, a well-known, phosphodiesterase-5 blocker, which act by potentiating the vasodilatory effect on smooth muscle relaxation, has never been studied in DCS. The purpose of the present study was to evaluate the clinical effects of sildenafil pre-treatment on DCS in a rat model. 67 rats were subjected to a simulated dive at 90 msw for 45 min before staged decompression. The experimental group received 10 mg/kg of sildenafil one hour before exposure (n = 35) while controls were not treated (n = 32). Clinical assessment took place over a period of 30 min after surfacing. At the end, blood samples were collected for blood cells counts and the level of circulating bubbles in the right cavities was quantified. There were significantly more manifestations of DCS in the sildenafil group than in the controls (34.3% vs 6.25%, respectively, p = 0.012). Platelet count was more reduced in treated rats than in controls (−21.7% vs −7%, respectively, p = 0.029), whereas bubble grades did not differ between groups. We concluded that pre-treatment with sildenafil promotes the onset and severity of neurological DCS. When considering the use of phosphodiesterase-5 blockers in the context of diving, careful discussion with physician should be recommended.
Highlights
Scuba diving is an activity growing in popularity every year
It is acknowledged that vascular bubble formation contribute to endothelial injury leading to vascular obstruction, microcirculatory alterations and activation of coagulation cascades, which may form the basis for the development of decompression sickness (DCS) [5,7]
There was significantly more neurological symptoms of DCS in the sildenafil group compared with the controls (34.3% vs 6.25%, respectively, p = 0.012)
Summary
Scuba (self contained underwater breathing apparatus) diving is an activity growing in popularity every year. Scuba diving may result in the production of bubbles due to the release of inert gas originally held in solution in the form of a free gas phase from peripheral tissues during decompression. When bubbles are excessively generated in blood and tissues, signs and symptoms referred to as decompression sickness (DCS) may occur [1]. It is generally accepted that gas bubbles grow from pre-formed gas nuclei attached to the vessel walls [2] and that venous gas emboli magnitude is linked to an increased risk of DCS [3,4]. Neurological damage in the spinal cord and brain underlies the most serious symptoms of DCS [5]. It is acknowledged that vascular bubble formation contribute to endothelial injury leading to vascular obstruction, microcirculatory alterations and activation of coagulation cascades, which may form the basis for the development of DCS [5,7]
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