Disease mechanisms which can be modelled with experimental hypoxia
Above 2000 meters, sleep in hypobaric and normobaric hypoxia produces a characteristic periodic breathing pattern, similar to central sleep apnea, which is called Cheyne-Stokes breathing (Figure 3). The apnea hypopnoea index is directly proportionally associated with increasing sleeping altitude whereas mean oxygen saturation during sleep is inversely associated [76].
Intermittent hypoxia, which mirrors the repetitive cycles of hypoxia and reoxygenation experienced by individuals with OSA during sleep can be used to model OSA. This modeling approach allows researchers to study the effects of intermittent hypoxia on various physiological processes. Oxidative stress, another important mechanism in OSA, can be replicated through hypoxia-induced imbalance between reactive oxygen species production and neutralization. Furthermore, hypoxia-induced inflammation and endothelial dysfunction, key contributors to OSA-related complications, can be investigated by simulating the inflammatory responses and impaired vascular function associated with hypoxia exposure. It is important for hypoxia models to accurately replicate the intermittent nature of hypoxia during sleep and consider the specific characteristics of OSA, including upper airway obstruction and sleep architecture. Controlling the duration and severity of hypoxia exposure is crucial to mimic the varying degrees of intermittent hypoxia observed in OSA patients. By employing hypoxia as a modeling tool, researchers can gain valuable insights into the underlying disease mechanisms of OSA and its associated complications, paving the way for the development of targeted therapeutic strategies.