Analysis Program, Division of Sleep Medicine, Brigham and Women’s Hospital
Research Plan, Division of Sleep Medicine, Brigham and Women’s Hospital and Harvard Medical College, Boston, MA 02115, USA. E mail: [email protected] Abbreviations AHI, apnoea ypopnoea index; CPAP, continuous constructive airway stress; CSA, central sleep apnoea; EEG, AT1 Receptor Agonist Accession electroencephalography; LG, loop gain; nREM, non-rapid eye movement; OSA, obstructive sleep apnoea; UAG, upper airway obtain; VRA, ventilatory response to spontaneous arousal.J Physiol 592.Introduction The pathophysiology of obstructive sleep apnoea (OSA) is multi-factorial. Many crucial elements, called physiological `traits’, happen to be shown to combine to bring about OSA. These involve: (i) poor upper airway anatomy that predisposes the airway to collapse; (ii) poor potential with the upper airway muscles to respond to a respiratory challenge and stiffen or dilate the airway; (iii) a low respiratory arousal threshold that causes a person to arouse from sleep for really small increases in respiratory drive, and (iv) a hypersensitive ventilatory handle technique frequently known as a technique with a high loop achieve (LG) (Gold et al. 1985; Wellman et al. 2011). Over the years, several investigators have examined the use of supplemental oxygen therapy as a therapy for OSA. However, the effects of supplemental oxygen on the severity of OSA and its consequences are extremely variable (Wellman et al. 2008; Mehta et al. 2013; Xie et al. 2013). Compact physiological studies indicate that oxygen therapy drastically improves the apnoea ypopnoea index (AHI) in 360 of people, whereas OSA severity remains unchanged or worsens in other sufferers. For those sufferers in whom supplemental oxygen is effective, it is actually likely that it improves OSA by minimizing the 5-HT3 Receptor Modulator Formulation sensitivity from the ventilatory control system (i.e. by decreasing LG) (Wellman et al. 2008; Xie et al. 2013). Nevertheless, like any drug, oxygen may have other crucial physiological effects. While oxygen may be able to decrease the sensitivity in the ventilatory handle technique, the reduction in ventilatory drive may have the unwanted effect of reducing the respiratory output towards the upper airway muscle tissues (Aleksandrova, 2004), which could potentially boost upper airway collapsibility and reduce pharyngeal dilator muscle responsiveness. Such a worsening of those traits may perhaps clarify why a proportion of OSA patients usually do not strengthen or actually worsen. By contrast, exposure to hypoxaemia, including that which may perhaps take place at altitude or in heart failure, has been clinically observed to change OSA to central sleep apnoea (CSA) (Warner et al. 1987; Burgess et al. 2004, 2006; Patz et al. 2006; Nussbaumer-Ochsner et al. 2010), which suggests that hypoxaemia may perhaps improve the upper airway anatomy or responsiveness as well as elevating LG. It really is properly documented that hypoxia will raise LG (Khoo et al. 1982; Solin et al. 2000; Sands et al. 2011; Andrews et al. 2012) andthat a higher LG amplifies tiny disturbances in ventilation, yielding cyclic oscillations in ventilatory drive, as seen in CSA. Having said that, in addition to raising LG, the conversion of OSA to CSA suggests that hypoxia might also strengthen the pharyngeal anatomy or responsiveness through an elevated drive to the upper airway muscles (Jordan et al. 2010). On the other hand, to date there has been no systematic investigation of how either hyperoxia or hypoxia alter the underlying physiology in sufferers with OSA. Accordingly, the aim of this study was to assess how modifications in oxygen levels alter the physiological.
