Exogenous Nitric Oxide and Bubble Formation in Divers

Dujić, Željko; Palada, Ivan; Valić, Zoran; Duplančić, Darko; Obad, Ante; Wisløff, Ulrik; Brubakk, Alf O.

doi:10.1249/01.mss.0000228936.78916.23

Cited by 52 publications

(47 citation statements)

References 16 publications

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“…Infusinġ NO donor drugs reduces injury in decompressed animals and decreases the number of intravascular bubbles in both animals and humans (6,23,34,39). Given the varied effects of˙NO these findings are not necessarily contradictory to observations in our study.…”

Section: Discussionsupporting

confidence: 50%

Intramicroparticle nitrogen dioxide is a bubble nucleation site leading to decompression-induced neutrophil activation and vascular injury

Thom

Yang

Bhopale

et al. 2013

Journal of Applied Physiology

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Inert gases diffuse into tissues in proportion to ambient pressure, and when pressure is reduced, gas efflux forms bubbles due to the presence of gas cavitation nuclei that are predicted based on theory but have never been characterized. Decompression stress triggers elevations in number and diameter of circulating annexin V-coated microparticles (MPs) derived from vascular cells. Here we show that ∼10% MPs from wild-type (WT) but not inflammatory nitric oxide synthase-2 (iNOS) knockout (KO) mice increase in size when exposed to elevated air pressure ex vivo. This response is abrogated by a preceding exposure to hydrostatic pressure, demonstrating the presence of a preformed gas phase. These MPs have lower density than most particles, 10-fold enrichment in iNOS, and generate commensurately more reactive nitrogen species (RNS). Surprisingly, RNS only slowly diffuse from within MPs unless particles are subjected to osmotic stress or membrane cholesterol is removed. WT mice treated with iNOS inhibitor and KO mice exhibit less decompression-induced neutrophil activation and vascular leak. Contrary to injecting naïve mice with MPs from wild-type decompressed mice, injecting KO MPs triggers fewer proinflammatory events. We conclude that nitrogen dioxide is a nascent gas nucleation site synthesized in some MPs and is responsible for initiating postdecompression inflammatory injuries.

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Section: Discussionsupporting

confidence: 50%

Intramicroparticle nitrogen dioxide is a bubble nucleation site leading to decompression-induced neutrophil activation and vascular injury

Thom

Yang

Bhopale

et al. 2013

Journal of Applied Physiology

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“…Many research efforts have focused on the role of nitric oxide as a marker of the general " health " of the endothelium and as a mediator of the hydrophilic/hydrophobic properties of the endothelial wall ( 8,13,23,38 ). Furthermore, the respiration of oxygen before the dive ( 9 ), or again, a short hyperbaric exposure ( 19,24 ), seems to be capable of reducing the nitrogen content of these nuclei and exerting a protective role on postdive VGE.…”

Section: Discussionmentioning

confidence: 99%

“…However, as our vibration sessions did not result in a signifi cant modifi cation of the endothelial reactivity, as indicated by the FMD measurements, we do not think NO production or vessel wall reactivity was signifi cantly altered in our study subjects. Previously it has been shown that administration of nitroglycerin prior to a dive may reduce bubble formation after the dive and the use of short-acting NO donors has been suggested as a protective measure ( 13 ). Whether the combination of NO donors and low-intensity vibration would lead to an even greater reduction in VGE remains to be investigated.…”

Section: Discussionmentioning

confidence: 99%

“…The general idea behind this approach is that post-dive decompression bubbles originate from the endothelial surface. Reports have been published on the benefi cial effects of pre-dive exercise ( 5,14 ), oxygen breathing ( 9 ), pre-dive hyperbaric sessions ( 19,24 ), heat preconditioning ( 6 ), hydration ( 15 ), and nitric oxide (NO) donor administration ( 13 ). Most of these experiments try to infl uence bubble formation by modifying biophysical or chemical properties of the endothelial surface, on which gas bubbles or nuclei are presumed to be forming.…”

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confidence: 99%

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Pre-Dive Vibration Effect on Bubble Formation After a 30-m Dive Requiring a Decompression Stop

Germonpré¹,

Pontier²,

Gempp³

et al. 2009

aviat space environ med

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G ERMONPRE P, PONTIER J-M, GEMPP E, BLATTEAU J-E, DENEWETH S, LAFÉRE P, MARRONIIntroduction: The preconditioning of divers to reduce post-dive decompression sickness (DCS) has gained increased interest in diving medical research over the last few years. The benefi cial effects of physical exercise, oxygen breathing, hyperbaric exposure, heat exposure, hyperhydration, or nitroglycerin administration before the dive are only a few examples of ongoing research. In this work, we investigated the effects of pre-dive whole-body vibration on post-dive bubble formation. Methods: Following French Navy standard dive procedures, 14 healthy male military divers performed 2 identical dives 1 wk apart to 30 m of seawater (msw) for 30 min. One of the dives was randomly preceded by a 30-min whole-body vibration session (frequencies 35-40 Hz) 1 h before the dive. Post-dive bubbles were measured precordially 30, 60, and 90 min after the dive and were graded according to the Kissman Integrated Severity Score (KISS) protocol, with and without knee fl exing. Arterial endothelial function was measured before and after vibration using fl ow mediated dilation (FMD) measurement. Results: A signifi cant reduction in bubble scores was observed after the " vibration " dive. Conclusion: As there was no observed change in FMD after vibration, we do not believe a nitric oxide mediated mechanism is involved; rather, a mechanical dislodgement or enhanced lymphatic elimination of gas nuclei is hypothesized.

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“…Nitric oxide (NO) might be involved in the prevention of bubble formation, the central goal in decompression procedures. The intake of an NO donor reduces bubble formation following decompression in divers [315].…”

Section: Treatmentmentioning

confidence: 99%

Nonthrombotic pulmonary embolism

Jorens¹,

Marck²,

Snoeckx³

et al. 2009

Eur Respir J

162

127

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Nonthrombotic pulmonary embolism (NTPE) is defined as embolisation to the pulmonary circulation of different cell types (adipocytes, haematopoietic, amniotic, trophoblastic or tumour), bacteria, fungi, foreign material or gas. The purpose of this article is to describe the clinical signs, pathogenesis, diagnosis and treatment of the different NTPE subtypes.The complex and diverse pathogenesis of different subtypes of emboli is subject to continuing speculation and is certainly far more complex than ''simple'' mechanical obstruction after embolisation of vascular thrombi. Nonthrombotic emboli may also lead to a severe inflammatory reaction both in the systemic and pulmonary circulation, as well as in the lung.NTPE presents a formidable diagnostic challenge, as the condition often presents with very unusual and peculiar clinical signs that are frequently overlooked. They range from very dramatic acute presentations such as acute respiratory distress syndrome to signs observed late in the disease course. Pathological observations play a key role in the exact diagnosis, and sometimes carefully aspirated blood from the pulmonary artery or specific staining of cells recovered from bronchoalveolar lavage fluid may be helpful. Frequently, lung biopsies revealing severe granulomatous reaction or unfortunate post-mortem pathological investigations of pulmonary tissue are necessary to confirm the diagnosis. Here, we also aim to familiarise the reader with the atypical radiological features of NTPE. Thin-section computed tomography of the lungs showing peculiar radiographic findings, such as a feeding vessel, the so-called tree-in-bud pattern or the appearance of micronodules distributed at the termination of bronchovascular bundles, may be observed in certain forms of NTPE.Increased awareness of NTPE as an underestimated cause of acute and chronic embolism, which may result in acute and chronic pulmonary hypertension, is needed. Despite the fact that detailed descriptions of several forms of NTPE have existed for nearly 100 years, well-designed trials have never been performed to evaluate therapy in the different subsets of these patients.

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Exogenous Nitric Oxide and Bubble Formation in Divers

Abstract: The present study demonstrates that intake of a short-lasting NO donor reduces bubble formation following decompression after different dives.

Cited by 52 publications

References 16 publications

Intramicroparticle nitrogen dioxide is a bubble nucleation site leading to decompression-induced neutrophil activation and vascular injury

Intramicroparticle nitrogen dioxide is a bubble nucleation site leading to decompression-induced neutrophil activation and vascular injury

Pre-Dive Vibration Effect on Bubble Formation After a 30-m Dive Requiring a Decompression Stop

Nonthrombotic pulmonary embolism

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