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Background: Hyperoxia-induced brain injury is a severe neurological complication that is often accompanied by adverse long-term prognosis. The pathogenesis of hyperoxia-induced brain injury is highly complex, with neuroinflammation playing a crucial role. The activation of the nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome, which plays a pivotal role in regulating and amplifying the inflammatory response, is the pathological core of hyperoxia-induced brain injury.

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Background: Bronchopulmonary dysplasia (BPD) is a chronic lung condition of premature neonates, yet without an established pharmacological treatment. The BPD rabbit model exposed to 95% oxygen has been used in recent years for drug testing. However, the toxicity of the strong hyperoxic hit precludes a longer-term follow-up due to high mortality after the first week of life.

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Arieli has previously demonstrated that the exposure metric K could be used to predict pulmonary oxygen toxicity (POT) based on changes in Vital Capacity (VC). Our previous findings indicate that the Equivalent Surface Oxygen Time (ESOT) allows the estimation of POT without loss of accuracy compared to K. In this work, we have further investigated POT recovery.

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Serotonin (5-HT) is integral to signalling in areas of the brainstem controlling ventilation and is involved in central chemoreception. Selective serotonin reuptake inhibitors (SSRIs), used to effectively increase 5-HT concentrations, are commonly prescribed for depression. The effects of SSRIs on the control of breathing and the potential influence of cerebral blood flow (CBF) have not been directly assessed.

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Introduction: A 54-year-old, previously healthy Caucasian male diver was on a 22-day liveaboard diving holiday. During this time, he performed 75 open-circuit dives, of which 72 were with enriched air nitrox. All dives were within recreational length and depth.

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