Respiratory physiology & neurobiology
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Respir Physiol Neurobiol · Sep 2013
ReviewThe impact of spinal cord injury on breathing during sleep.
The prevalence of sleep disordered breathing (SDB) following spinal cord injury (SCI) is considerably greater than in the general population. While the literature on this topic is still relatively small, and in some cases contradictory, a few general conclusions can be drawn. ⋯ It is not yet possible to pinpoint a "primary factor" which will predispose an individual with SCI to SDB, and the underlying mechanisms may change during progression from acute to chronic injury. Given the prevalence and potential health implications of SDB in the SCI population, we suggest that additional studies aimed at defining the underlying mechanisms are warranted.
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Respir Physiol Neurobiol · Sep 2013
ReviewK+ channel modulation causes genioglossus inhibition in REM sleep and is a strategy for reactivation.
Rapid eye movement (REM) sleep is accompanied by periods of upper airway motor suppression that cause hypoventilation and obstructive apneas in susceptible individuals. A common idea has been that upper airway motor suppression in REM sleep is caused by the neurotransmitters glycine and γ-amino butyric acid (GABA) acting at pharyngeal motor pools to inhibit motoneuron activity. ⋯ We then outline how this discovery informs efforts to pursue therapeutic targets to reactivate hypoglossal motor activity throughout sleep via potassium channel modulation. One such target is the inwardly rectifying potassium channel Kir2.4 whose expression in the brain is almost exclusive to cranial motor nuclei.
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We provide an updated review on the current understanding of breathing and sleep at high altitude in humans. We conclude that: (1) progressive changes in pH initiated by the respiratory alkalosis do not underlie early (<48 h) ventilatory acclimatization to hypoxia (VAH) because this still proceeds in the absence of such alkalosis; (2) for VAH of longer duration (>48 h), complex cellular and neurochemical re-organization occurs both in the peripheral chemoreceptors as well as within the central nervous system. The latter is likely influenced by central acid-base changes secondary to the extent of the initial respiratory responses to initial exposure to high altitude; (3) sleep at high altitude is disturbed by various factors, but principally by periodic breathing; (4) the extent of periodic breathing during sleep at altitude intensifies with duration and severity of exposure; (5) complex interactions between hypoxic-induced enhancement in peripheral and central chemoreflexes and cerebral blood flow--leading to higher loop gain and breathing instability--underpin this development of periodic breathing during sleep; (6) because periodic breathing may elevate rather than reduce mean SaO2 during sleep, this may represent an adaptive rather than maladaptive response; (7) although oral acetazolamide is an effective means to reduce periodic breathing by 50-80%, recent studies using positive airway pressure devices to increase dead space, hyponotics and theophylline are emerging but appear less practical and effective compared to acetazolamide. Finally, we suggest avenues for future research, and discuss implications for understanding sleep pathology.
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Respir Physiol Neurobiol · Sep 2013
ReviewBreathing and brain state: urethane anesthesia as a model for natural sleep.
Respiratory control differs dramatically across sleep stages. Indeed, along with rapid eye movements (REM), respiration was one of the first physiological variables shown to be modulated across sleep stages. ⋯ We describe this model, its parallels with natural sleep, and its power for studying modulation of respiration. Specifically, we report data on the EEG characteristics across brain states under urethane anesthesia, the dependence of brain alternations on neurotransmitter systems, and the observations on state dependent modulation of respiration.
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Respir Physiol Neurobiol · Aug 2013
Validity of arterialised-venous P CO2, pH and bicarbonate in obesity hypoventilation syndrome.
This prospective study investigated the validity of arterialised-venous blood gases (AVBG) for estimating arterial carbon dioxide P CO2, pH and bicarbonate (HCO3(-)) in people with obesity hypoventilation syndrome (OHS). AVBGs were obtained from an upper limb vein, after heating the skin at 42-46°C. Arterial blood gas (ABG) and AVBG samples were taken simultaneously and compared using Bland Altman analysis. ⋯ Forty-two viable paired samples were analysed, including 27 paired samples from 15 OHS participants, and 15 paired samples from 16 controls. AVBG-ABG agreement was not different between groups, or between dorsal hand, forearm and antecubital AVBG sampling sites, and was clinically acceptable for P Co2: mean difference (MD) 0.4 mmHg (0.9%), limits of agreement (LOA) -2.7-3.6 mmHg (± 6.6%); pH: MD -0.008 (-0.1%), LOA -0.023-0.008 (± 0.2%); and HCO3(-): MD -0.3 mmol L(-1) (-1.0%), LOA -1.8-1.2 mmol L(-1) (± 5.3%). AVBG provides valid measures of [Formula: see text] , pH, and HCO3(-) in OHS.