Exhaled nitric oxide concentration and decompression-induced bubble formation: An index of decompression severity in humans?

INTRODUCTION: Previous studies have highlighted a decreased exhaled nitric oxide concentration (FE NO) in divers after hyperbaric exposure in a dry chamber or following a wet dive. The underlying mechanisms of this decrease remain however unknown. The aim of this study was to quantify the separate effects of submersion, hyperbaric hyperoxia exposure and decompression-induced bubble formation on FE NO after a wet dive. METHODS: Healthy experienced divers (n=31) were assigned to either (i) a group making a scuba-air dive (Air dive), (ii) a group with a shallow oxygen dive protocol (Oxygen dive) or (iii) a group making a deep dive breathing a trimix gas mixture (deep-dive). Bubble signals were graded with the KISS score. Before and after each dive FE NO values were measured using a hand-held electrochemical analyzer. RESULTS: There was no change in post-dive values of FE NO values (expressed in ppb=parts per billion) in the Air dive group (15.1 ± 3.6 ppb vs. 14.3 ± 4.7 ppb, n=9, p=0.32). There was a significant decrease in post-dive values of FE NO in the Oxygen dive group (15.6 ± 6 ppb vs. 11.7 ± 4.7 ppb, n=9, p=0.009). There was an even more pronounced decrease in the deep dive group (16.4 ± 6.6 ppb vs. 9.4 ± 3.5 ppb, n=13, p<0.001) and a significant correlation between KISS bubble score >0 (n=13) and percentage decrease in post-dive FE NO values (r=-0.53, p=0.03). DISCUSSION: Submersion and hyperbaric hyperoxia exposure cannot account entirely for these results suggesting the possibility that, in combination, one effect magnifies the other. A main finding of the present study is a significant relationship between reduction in exhaled NO concentration and dive-induced bubble formation. We postulate that exhaled NO concentration could be a useful index of decompression severity in healthy human divers.

Effect of oxygen-breathing during a decompression-stop on bubble-induced platelet activation after an open-sea air dive: oxygen-stop decompression.

PURPOSE: We highlighted a relationship between decompression-induced bubble formation and platelet micro-particle (PMP) release after a scuba air-dive. It is known that decompression protocol using oxygen-stop accelerates the washout of nitrogen loaded in tissues. The aim was to study the effect of oxygen deco-stop on bubble formation and cell-derived MP release. METHODS: Healthy experienced divers performed two scuba-air dives to 30 msw for 30 min, one with an air deco-stop and a second with 100% oxygen deco-stop at 3 msw for 9 min. Bubble grades were monitored with ultrasound and converted to the Kisman integrated severity score (KISS). Blood samples for cell-derived micro-particle analysis (AnnexinV for PMP and CD31 for endothelial MP) were taken 1 h before and after each dive. RESULTS: Mean KISS bubble score was significantly lower after the dive with oxygen-decompression stop, compared to the dive with air-decompression stop (4.3 ± 7.3 vs. 32.7 ± 19.9, p < 0.001). After the dive with an air-breathing decompression stop, we observed an increase of the post-dive mean values of PMP (753 ± 245 vs. 381 ± 191 ng/µl, p = 0.003) but no significant change in the oxygen-stop decompression dive (329 ± 215 vs. 381 +/191 ng/µl, p = 0.2). For the post-dive mean values of endothelial MP, there was no significant difference between both the dives. CONCLUSIONS: The Oxygen breathing during decompression has a beneficial effect on bubble formation accelerating the washout of nitrogen loaded in tissues. Secondary oxygen-decompression stop could reduce bubble-induced platelet activation and the pro-coagulant activity of PMP release preventing the thrombotic event in the pathogenesis of decompression sickness.

Influence of decompression sickness on vasomotion of isolated rat vessels.

Several studies have demonstrated that endothelial function is impaired following a dive even without decompression sickness. During this study we determined the effect of decompression sickness on endothelium-dependent and independent vasoreactivity. For this purpose twenty-seven male Sprague-Dawley rats were submitted to a simulated dive up to 1,000 kPa absolute pressure and divided into 3 groups: safe diving without decompression sickness or dives provoking mild or severe sickness. A fourth control group remained at atmospheric pressure. Endothelium-dependent and independent vasomotion was assessed ex vivo by measuring isometric tension in rings of abdominal aorta and mesenteric arteries. Dose-response curves were obtained with phenylephrine, acetylcholine and sodium nitroprusside. Acetylcholine-induced relaxation was measured in the presence of L-NAME, indometacin or both of them at once.Contraction was significantly decreased after each protocol compared with the control rats. Additionally, the response in animals from the severe group was significantly different from that of the safe and mild groups. Dose response curves for acetylcholine alone and in the presence of inhibitors remained unchanged. We did not observe differences in endothelium-dependent vasodilation after diving or in the presence of decompression sickness. Contractile response to phenylephrine was progressively impaired with increased decompression stress. These results may indicate smooth muscle injury.