Abstract
We previously showed microvascular alteration of both endothelium-dependent and -independent reactivity after a single SCUBA dive. We aimed to study mechanisms involved in this postdive vascular dysfunction. Ten divers each completed three protocols: (1) a SCUBA dive at 400 kPa for 30 min; (2) a 41-min duration of seawater surface head immersed finning exercise to determine the effect of immersion and moderate physical activity; and (3) a simulated 41-min dive breathing 100% oxygen (hyperbaric oxygen [HBO]) at 170 kPa in order to analyze the effect of diving-induced hyperoxia. Bubble grades were monitored with Doppler. Cutaneous microvascular function was assessed by laser Doppler. Endothelium-dependent (acetylcholine, ACh) and -independent (sodium nitroprusside, SNP) reactivity was tested by iontophoresis. Endothelial cell activation was quantified by plasma Von Willebrand factor and nitric oxide (NO). Inactivation of NO by oxidative stress was assessed by plasma nitrotyrosine. Platelet factor 4 (PF4) was assessed in order to determine platelet aggregation. Blood was also analyzed for measurement of platelet count. Cutaneous vascular conductance (CVC) response to ACh delivery was not significantly decreased by the SCUBA protocol (23 ± 9% before vs. 17 ± 7% after; P = 0.122), whereas CVC response to SNP stimulation decreased significantly (23 ± 6% before vs. 10 ± 1% after; P = 0.039). The HBO and immersion protocols did not affect either endothelial-dependent or -independent function. The immersion protocol induced a significant increase in NO (0.07 ± 0.01 vs. 0.12 ± 0.02 μg/mL; P = 0.035). This study highlighted change in microvascular endothelial-independent but not -dependent function in highly trained divers after a single air dive. The results suggest that the effects of decompression on microvascular function may be modified by diving acclimatization.
Highlights
During decompression sickness (DCS) inert gas supersaturation results in the formation of intravascular bubbles which can lead to venous gas emboli (VGE)
None of the divers showed any symptoms of DCS in the SCUBA protocol
The first aim was to study human microvascular endothelial function in peripheral circulation of highly trained healthy divers after an open-sea air dive using laser Doppler flowmetry (LDF) and iontophoresis, and to relate these modifications to bubbleinduced platelet aggregation, endothelial activation/damage, and oxidative stress using the measurements of specific plasmatic markers
Summary
During decompression sickness (DCS) inert gas (usually nitrogen) supersaturation results in the formation of intravascular bubbles which can lead to venous gas emboli (VGE). It has been assumed that venous bubbles will be trapped in the pulmonary circulation and have no further effects on the arterial circulation. In most cases VGE occur without acute clinical symptom of DCS, decompressioninduced bubble formation is the pivotal event in DCS. Recent literature showed implication of different postdive pathophysiological events as endothelium dysfunction, coagulation, and inflammation processes that could play a substantial role in the occurrence of DCS. Circulating bubbles affect the clotting system both through activation of the coagulation cascade and the induction of platelet aggregation (Pontier et al 2009b)
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