Coordinated activation of sympathetic and respiratory nervous systems is crucial in responses to noxious stimuli such as intermittent hypoxia. Acute intermittent hypoxia (AIH) is a valuable model for studying obstructive sleep apnea (OSA) pathophysiology, and stimulation of breathing during AIH is known to elicit long-term changes in respiratory and sympathetic functions. The aim of this study was to record the renal sympathetic nerve activity (RSNA) and phrenic nerve activity (PNA) during the AIH protocol in rats exposed to monoanesthesia with sevoflurane or isoflurane. Adult male Sprague-Dawley rats ( = 24; weight: 280-360 g) were selected and randomly divided into three groups: two experimental groups (sevoflurane group, = 6; isoflurane group, = 6) and a control group (urethane group, = 12). The AIH protocol was identical in all studied groups and consisted in delivering five 3 min-long hypoxic episodes (fraction of inspired oxygen, FiO = 0.09), separated by 3 min recovery intervals at FiO = 0.5. Volatile anesthetics, isoflurane and sevoflurane, blunted the RSNA response to AIH in comparison to urethane anesthesia. Additionally, the PNA response to acute intermittent hypoxia was preserved, indicating that the respiratory system might be more robust than the sympathetic system response during exposure to acute intermittent hypoxia.
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http://dx.doi.org/10.3390/biomedicines12040910 | DOI Listing |
BMJ Open
December 2024
Department of Otolaryngology-Head and Neck Surgery, Vanderbilt University Medical Center, Nashville, Tennessee, USA
Introduction: Obstructive sleep apnoea (OSA) is characterised by blood oxygen desaturations and sleep disruptions manifesting undesirable consequences. Existing treatments including oral appliances, positive airway pressure (PAP) therapy and surgically altering the anatomy of the pharynx have drawbacks including poor long-term adherence or often involving irreversible, invasive procedures. Bilateral hypoglossal nerve stimulation (HNS) is a new treatment for managing OSA, and this study is intended to determine whether an HNS system is a safe and effective treatment option for adults with OSA.
View Article and Find Full Text PDFRespir Res
January 2025
Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Background: Obstructive sleep apnea (OSA) is frequently associated with increased incidence and mortality of pulmonary hypertension (PH). The immune response contributes to pulmonary artery remodeling and OSA-related diseases. The immunologic factors linked to OSA-induced PH are not well understood.
View Article and Find Full Text PDFJ Basic Clin Physiol Pharmacol
January 2025
Pharmacology, MGM Medical College and Hospital, MGM Institute of Health Sciences, Nerul, Navi Mumbai, Maharashtra, India.
Obstructive Sleep Apnea (OSA) is a prevalent sleep disorder marked by repeated episodes of partial or complete upper airway obstruction during sleep, which leads to intermittent hypoxia and fragmented sleep. These disruptions negatively impact cardiovascular health, metabolic function, and overall quality of life. Obesity is a major modifiable risk factor for OSA, as it contributes to both anatomical and physiological mechanisms that increase the likelihood of airway collapse during sleep.
View Article and Find Full Text PDFAm J Physiol Endocrinol Metab
January 2025
Division of Pulmonary, Critical Care, and Sleep Medicine, University of Miami, Miller School of Medicine, Miami Florida.
Intermittent hypoxemia (IH), a pathophysiologic consequence of obstructive sleep apnea (OSA), adversely affects insulin sensitivity, insulin secretion, and glucose tolerance. Nifedipine, an L-type calcium channel blocker frequently used for treatment of hypertension, can also impair insulin sensitivity and secretion. However, the cumulative and interactive repercussions of IH and nifedipine on glucose homeostasis have not been previously investigated.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Psychiatry and Behavioral Sciences, School of Medicine, Stanford University, 401 Quarry Road, Stanford, CA, 94305, USA.
Background: Intermittent hypoxia, a consequence of sleep-disordered breathing (SDB), may contribute to an increased risk of cognitive decline. However, the association between SDB and cognition remains highly variable.
Methods: Fifty-two community-dwelling healthy older adults (28 women) were recruited.
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