Venous gas emboli are involved in post-dive macro, but not microvascular dysfunction

Lambrechts, Kate; Balestra, Costantino; Théron, Michaël; Henckes, Anne; Galinat, Hubert; Mignant, Fanny; Belhomme, Marc; Pontier, Jean-Michel; Guerrero, François

doi:10.1007/s00421-017-3537-9

Cited by 21 publications

(25 citation statements)

References 44 publications

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“…In recent years, increasing studies focus on the influence of decompression-induced bubbles on vascular function and confirm that bubbles may cause damage to vascular endothelial cells, inducing vascular dysfunction. 19 20 21 This has been validated in our studies. 22 23 In addition, the improvement of vascular function was also found to be protective on DCS.…”

Section: E Vidence On the R Ole Of supporting

confidence: 67%

Macrophage polarization is related to the pathogenesis of decompression induced lung injury

Han

Zhang²,

Liu³

2017

Med Gas Res

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Studies have shown that blood bubbles may be detectable and there is ultrasonic evidence of acute interstitial lung edema even after diving without protocol violation. Macrophages play a central role in the inflammation, and macrophage polarization is closely related to the pathogenesis some lung diseases. Available findings indicate that decompression may induce the production of pro-inflammatory cytokines, chemokines, and adhesion molecules in the blood and tissues, which are associated with the macrophage polarization, and hyperbaric treatment may exert therapeutic effects on decompression related diseases via regulating these factors. Thus, we hypothesize that the polarization of circulating and/or resident macrophages is involved in the pathogenesis of decompression induced lung injury.

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Section: E Vidence On the R Ole Of supporting

confidence: 67%

Macrophage polarization is related to the pathogenesis of decompression induced lung injury

Han

Zhang²,

Liu³

2017

Med Gas Res

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“…With the influx of inert gases, these MPs become larger and further increase stress and related injuries (Brugniaux et al 2018). Bubbles in turn could also activate hemostatic pathways and induce increases in circulating MPs, which could further impair arterial endothelial function (Lambrechts et al 2017). Also, diving-related changes in NO could activate processes like platelet activation, leukocyte adhesion, and thrombosis (Cialoni et al 2019).…”

Section: Discussionmentioning

confidence: 99%

Vascular dysfunction following breath-hold diving

Barak

Janjic

Drviš

et al. 2020

Can. J. Physiol. Pharmacol.

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The pathogenesis of predominantly neurological decompression sickness (DCS) is multifactorial. In SCUBA diving, besides gas bubbles, DCS has been linked to microparticle release, impaired endothelial function, and platelet activation. This study focused on vascular damage and its potential role in the genesis of DCS in breath-hold diving. Eleven breath-hold divers participated in a field study comprising eight deep breath-hold dives with short surface periods and repetitive breath-hold dives lasting for 6 h. Endothelium-dependent vasodilation of the brachial artery, via flow-mediated dilation (FMD), and the number of microparticles (MPs) were assessed before and after each protocol. All measures were analyzed by two-way within-subject ANOVA (2 × 2 ANOVA; factors: time and protocol). Absolute FMD was reduced following both diving protocols (p < 0.001), with no interaction (p = 0.288) or main effect of protocol (p = 0.151). There was a significant difference in the total number of circulating MPs between protocols (p = 0.007), where both increased post-dive (p = 0.012). The number of CD31+/CD41– and CD66b+ MP subtypes, although different between protocols (p < 0.001), also increased by 41.0% ± 56.6% (p = 0.050) and 60.0% ± 53.2% (p = 0.045) following deep and repetitive breath-hold dives, respectively. Both deep and repetitive breath-hold diving lead to endothelial dysfunction that may play an important role in the genesis of neurological DCS.

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“…The air embolism has been well studied when a bubble is trapped in a vessel and contacts the endothelial layer (11)(12)(13). However, it is still unclear how a bubble moving along with the continuous blood flow stops in the vessel.…”

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confidence: 99%

Flow field around bubbles on formation of air embolism in small vessels

et al. 2021

Proc. Natl. Acad. Sci. U.S.A.

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An air embolism is induced by intravascular bubbles that block the blood flow in vessels, which causes a high risk of pulmonary hypertension and myocardial and cerebral infarction. However, it is still unclear how a moving bubble is stopped in the blood flow to form an air embolism in small vessels. In this work, microfluidic experiments, in vivo and in vitro, are performed in small vessels, where bubbles are seen to deform and stop gradually in the flow. A clot is always found to originate at the tail of a moving bubble, which is attributed to the special flow field around the bubble. As the clot grows, it breaks the lubrication film between the bubble and the channel wall; thus, the friction force is increased to stop the bubble. This study illustrates the stopping process of elongated bubbles in small vessels and brings insight into the formation of air embolism.

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Venous gas emboli are involved in post-dive macro, but not microvascular dysfunction

Abstract: Finally, the results of this study suggest that macro- but not microvascular impairment results at least partly from bubbles, possibly related to platelet activation and generation of pro-coagulant microparticles.

Cited by 21 publications

References 44 publications

Macrophage polarization is related to the pathogenesis of decompression induced lung injury

Macrophage polarization is related to the pathogenesis of decompression induced lung injury

Vascular dysfunction following breath-hold diving

Flow field around bubbles on formation of air embolism in small vessels

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