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Daytime sympathetic hyperactivity in OSAS is related to excessive daytime sleepiness.

Donadio, Vincenzo (författare)
Liguori, Rocco (författare)
Vetrugno, Roberto (författare)
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Contin, Manuela (författare)
Elam, Mikael, 1956 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering,Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation
Wallin, Gunnar B, 1936 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering,Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation
Karlsson, Tomas, 1957 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering,Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation
Bugiardini, Enrico (författare)
Baruzzi, Agostino (författare)
Montagna, Pasquale (författare)
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2007
2007
Engelska.
Ingår i: Journal of sleep research. - 0962-1105. ; 16:3, s. 327-32
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
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  • The aim of this study was to investigate the relationships among sympathetic hyperactivity, excessive daytime sleepiness (EDS) and hypertension in obstructive sleep apnoea syndrome (OSAS). Ten newly diagnosed OSAS patients with untreated EDS and daytime hypertension underwent polysomnography (PSG) and daytime measurements of plasma noradrenaline (NA), ambulatory blood pressure (BP), muscle sympathetic nerve activity (MSNA) by microneurography and objective assessment of EDS before and during 6 months of compliance-monitored continuous positive airway pressure (CPAP) treatment. One month after the start of CPAP, BP, MSNA and NA were significantly lowered, remaining lower than baseline also after 3 and 6 months of treatment. CPAP use caused a significant improvement of sleep structures, and reduced EDS. A statistical correlation analysis demonstrated that EDS was not correlated with sleep measures obtained from baseline PSG (% sleep stages, apnoea and arousal index, mean oxygen saturation value), whereas daytime sleepiness was significantly correlated with MSNA. Furthermore, MSNA and BP showed no correlation. Our data obtained from selected patients suggest that the mechanisms inducing EDS in OSAS are related to the degree of daytime sympathetic hyperactivity. Additionally, resting MSNA was unrelated to BP suggesting that factors other than adrenergic neural tone make a major contribution to OSAS-related hypertension. The results obtained in this pilot study need, however, to be confirmed in a larger study involving more patients.

Nyckelord

Animals
Continuous Positive Airway Pressure
Disorders of Excessive Somnolence
complications
etiology
physiopathology
Female
Humans
Hyperkinesis
complications
physiopathology
Hypertension
complications
Male
Middle Aged
Muscle
Skeletal
innervation
Polysomnography
Rabbits
Sleep Apnea
Obstructive
complications
physiopathology
Sympathetic Nervous System
physiopathology
Treatment Outcome

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