Blood pressure in rats selectively bred for their resistance to decompression sickness

Dugrenot, Emmanuel; Orsat, Jérémy; Guerrero, François

doi:10.28920/dhm52.2.119-125

Cited by 3 publications

(1 citation statement)

References 29 publications

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“…Moreover, it has been reported that captopril, an ACE inhibitor, could significantly ameliorate endothelial dysfunction caused by irradiation 20 . In DCS patients, the plasma level of Ang II was also increased 21 , 22 . The above studies highlighted the importance of Ang II in vascular damage and inflammation in irradiation and DCS.…”

Section: Introductionmentioning

confidence: 92%

Effect of angiotensin II on irradiation exacerbated decompression sickness

Fan

Wang

Liu

et al. 2023

Sci Rep

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In some complicated situations, decompression sickness (DCS) combined with other injuries, such as irradiation, will seriously endanger life safety. However, it is still unclear whether irradiation will increase the incidence of DCS. This study was designed to investigate the damage effects of irradiation on decompression injury and the underlying mechanism. Sprague–Dawley rats were exposed to irradiation followed by hyperbaric decompressing and the mortality and decompression symptoms were observed. Lung tissue and bronchoalveolar lavage fluid were collected to detect the lung lesion, inflammation response, activity of the angiotensin system, oxidative stress, and relative signal pathway by multiple methods, including Q-PCR, western blot, and ELISA. As a result, pre-exposure to radiation significantly exacerbated disease outcomes and lung lesions of DCS. Mechanically, the up-regulation of angiotensin-converting enzyme expression and angiotensin II levels was responsible for the exacerbated DCS and lung lesions caused by predisposing irradiation exposure. Oxidative stress and PI3K/AKT signal pathway activation in pulmonary tissue were enhanced after irradiation plus decompression treatment. In conclusion, our results suggested that irradiation could exacerbate lung injury and the outcomes of DCS by activating the angiotensin system, which included eliciting oxidative stress and activation of the PI3K/AKT signal pathway.

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Section: Introductionmentioning

confidence: 92%

Effect of angiotensin II on irradiation exacerbated decompression sickness

Fan

Wang

Liu

et al. 2023

Sci Rep

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Gene expression of Decompression Sickness-resistant rats through a miRnome/transcriptome crossed approach

Dugrenot,

Guernec,

Orsat

et al. 2024

Commun Biol

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Susceptibility to decompression sickness (DCS) is characterized by a wide inter-individual variability, the origins of which are still poorly understood. We selectively bred rats with at least a 3-fold greater resistance to DCS than standard rats after 6 generations. In order to better understand DCS mechanisms, we compared the static genome expression of these resistant rats from the 10 th generation to their counterparts of the initial non-resistant Wistar strain, by a microarray transcriptomic approach coupled and crossed with a PCR plates miRnome study. Thus, we identified differentially expressed genes on selected males and females, as well as gender differences in those genes, and we crossed these transcripts with the respective targets of the differentially expressed microRNAs. Our results highlight pathways involved in inflammatory responses, circadian clock, cell signaling and motricity, phagocytosis or apoptosis, and they confirm the importance of inflammation in DCS pathophysiology.

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Decompression illness: a comprehensive overview

Mitchell

2024

Diving Hyperb Med

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Decompression illness is a collective term for two maladies (decompression sickness [DCS] and arterial gas embolism [AGE]) that may arise during or after surfacing from compressed gas diving. Bubbles are the presumed primary vector of injury in both disorders, but the respective sources of bubbles are distinct. In DCS bubbles form primarily from inert gas that becomes dissolved in tissues over the course of a compressed gas dive. During and after ascent (‘decompression’), if the pressure of this dissolved gas exceeds ambient pressure small bubbles may form in the extravascular space or in tissue blood vessels, thereafter passing into the venous circulation. In AGE, if compressed gas is trapped in the lungs during ascent, pulmonary barotrauma may introduce bubbles directly into the pulmonary veins and thence to the systemic arterial circulation. In both settings, bubbles may provoke ischaemic, inflammatory, and mechanical injury to tissues and their associated microcirculation. While AGE typically presents with stroke-like manifestations referrable to cerebral involvement, DCS can affect many organs including the brain, spinal cord, inner ear, musculoskeletal tissue, cardiopulmonary system and skin, and potential symptoms are protean in both nature and severity. This comprehensive overview addresses the pathophysiology, manifestations, prevention and treatment of both disorders.

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Blood pressure in rats selectively bred for their resistance to decompression sickness

Cited by 3 publications

References 29 publications

Effect of angiotensin II on irradiation exacerbated decompression sickness

Effect of angiotensin II on irradiation exacerbated decompression sickness

Gene expression of Decompression Sickness-resistant rats through a miRnome/transcriptome crossed approach

Decompression illness: a comprehensive overview

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