Acute Effects on the Human Peripheral Blood Transcriptome of Decompression Sickness Secondary to Scuba Diving

Magri, Kurt; Eftedal, Ingrid; Magri, Vanessa Petroni; Matity, Lyubisa; Azzopardi, Charles Paul; Muscat, Stephen; Pace, Nikolai Paul

doi:10.3389/fphys.2021.660402

Cited by 14 publications

(8 citation statements)

References 96 publications

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“…While the role of MPs in decompression stress is not clear, they seem to play a major role as VGE precursors or as a mediator of inflammation [ 62 ]. To the best of our knowledge, this is the first study describing blood-borne MP responses to different PO 2 .…”

Section: Discussionmentioning

confidence: 99%

Varying Oxygen Partial Pressure Elicits Blood-Borne Microparticles Expressing Different Cell-Specific Proteins—Toward a Targeted Use of Oxygen?

Balestra

Arya

Leveque

et al. 2022

IJMS

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Oxygen is a powerful trigger for cellular reactions, but there are few comparative investigations assessing the effects over a large range of partial pressures. We investigated a metabolic response to single exposures to either normobaric (10%, 15%, 30%, 100%) or hyperbaric (1.4 ATA, 2.5 ATA) oxygen. Forty-eight healthy subjects (32 males/16 females; age: 43.7 ± 13.4 years, height: 172.7 ± 10.07 cm; weight 68.4 ± 15.7 kg) were randomly assigned, and blood samples were taken before and 2 h after each exposure. Microparticles (MPs) expressing proteins specific to different cells were analyzed, including platelets (CD41), neutrophils (CD66b), endothelial cells (CD146), and microglia (TMEM). Phalloidin binding and thrombospondin-1 (TSP), which are related to neutrophil and platelet activation, respectively, were also analyzed. The responses were found to be different and sometimes opposite. Significant elevations were identified for MPs expressing CD41, CD66b, TMEM, and phalloidin binding in all conditions but for 1.4 ATA, which elicited significant decreases. Few changes were found for CD146 and TSP. Regarding OPB, further investigation is needed to fully understand the future applications of such findings.

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Section: Discussionmentioning

confidence: 99%

Varying Oxygen Partial Pressure Elicits Blood-Borne Microparticles Expressing Different Cell-Specific Proteins—Toward a Targeted Use of Oxygen?

Balestra

Arya

Leveque

et al. 2022

IJMS

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“…While thromboinflammation has been well described in autoimmune disease, infectious disease, and COVID-19associated coagulopathy (131,132), there is little research into the thromboinflammatory effects of air emboli in humans. The exact mechanism by which activation of thromboinflammation and the effect of complement inhibition, for example, on thromboinflammation has previously been studied in in vitro human whole blood and in in vivo animal models (22,(133)(134)(135)(136). In an in vitro model of air emboli using lepirudinanticoagulated human whole blood (32) and in an in vivo porcine model (35), air emboli activated complement component 3 (C3) and triggered thromboinflammation.…”

Section: Thromboinflammation: Hydrodynamics Of Bubble Obstructionmentioning

confidence: 99%

Iatrogenic air embolism: pathoanatomy, thromboinflammation, endotheliopathy, and therapies

Marsh,

Moore,

Moore

et al. 2023

Front. Immunol.

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Iatrogenic vascular air embolism is a relatively infrequent event but is associated with significant morbidity and mortality. These emboli can arise in many clinical settings such as neurosurgery, cardiac surgery, and liver transplantation, but more recently, endoscopy, hemodialysis, thoracentesis, tissue biopsy, angiography, and central and peripheral venous access and removal have overtaken surgery and trauma as significant causes of vascular air embolism. The true incidence may be greater since many of these air emboli are asymptomatic and frequently go undiagnosed or unreported. Due to the rarity of vascular air embolism and because of the many manifestations, diagnoses can be difficult and require immediate therapeutic intervention. An iatrogenic air embolism can result in both venous and arterial emboli whose anatomic locations dictate the clinical course. Most clinically significant iatrogenic air emboli are caused by arterial obstruction of small vessels because the pulmonary gas exchange filters the more frequent, smaller volume bubbles that gain access to the venous circulation. However, there is a subset of patients with venous air emboli caused by larger volumes of air who present with more protean manifestations. There have been significant gains in the understanding of the interactions of fluid dynamics, hemostasis, and inflammation caused by air emboli due to in vitro and in vivo studies on flow dynamics of bubbles in small vessels. Intensive research regarding the thromboinflammatory changes at the level of the endothelium has been described recently. The obstruction of vessels by air emboli causes immediate pathoanatomic and immunologic and thromboinflammatory responses at the level of the endothelium. In this review, we describe those immunologic and thromboinflammatory responses at the level of the endothelium as well as evaluate traditional and novel forms of therapy for this rare and often unrecognized clinical condition.

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“…Transcriptome analysis of divers with DCS could also help to the better comprehension of this disease. 57 Regarding the role of PFO closure for secondary prevention of DCI, no randomized controlled study has compared the invasive versus conventional management. In addition, more studies about the risk stratification of divers with PFO should be conducted.…”

Section: Future Perspectivesmentioning

confidence: 99%

“…Transcriptome analysis of divers with DCS could also help to the better comprehension of this disease. 57 Regarding the role of…”

Section: Future Perspectivesmentioning

confidence: 99%

The management of patent foramen ovale in divers: where do we stand?

Toutouzas

Drakopoulou

Trantalis

et al. 2022

Ther Adv Neurol Disord

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Diving is a fascinating activity, but it does not come without any cost; decompression illness (DCI) is one of the most frequent diseases occurring in divers. Rapid surfacing after diving causes alveolar rupture and bubbles release, which enter in the systemic circulation and could embolize numerous organs and tissues. The presence of patent foramen ovale (PFO) contributes to the passage of venous gas bubbles into the arterial circulation, increasing the risk of complications related to DCI. The diagnosis is established with a detailed medical history, a comprehensive clinical evaluation, and a multimodal imaging approach. Although the percutaneous closure of PFO is ambiguous for divers, as a primary prevention strategy, transcatheter management is considered as beneficial for DCI recurrence prevention. The aim of this study is to introduce the basic principles of DCI, to review the pathophysiological connection between DCI and PFO, to highlight the risk factors and the optimal treatment, and, last but not least, to shed light on the role of closure as primary and secondary prevention.

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Acute Effects on the Human Peripheral Blood Transcriptome of Decompression Sickness Secondary to Scuba Diving

Cited by 14 publications

References 96 publications

Varying Oxygen Partial Pressure Elicits Blood-Borne Microparticles Expressing Different Cell-Specific Proteins—Toward a Targeted Use of Oxygen?

Varying Oxygen Partial Pressure Elicits Blood-Borne Microparticles Expressing Different Cell-Specific Proteins—Toward a Targeted Use of Oxygen?

Iatrogenic air embolism: pathoanatomy, thromboinflammation, endotheliopathy, and therapies

The management of patent foramen ovale in divers: where do we stand?

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