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.