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Related Concept Videos

Insufficient Sleep and Sleep Deprivation01:13

Insufficient Sleep and Sleep Deprivation

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Insufficient sleep refers to not getting the recommended amount of sleep for optimal functioning, even if it's just slightly less than needed. Sleep insufficiency may occur due to lifestyle choices, such as staying up late for social events or work, resulting in routinely getting less sleep than required. For example, consistently sleeping 6 hours when the body needs 7-9 hours can lead to cumulative effects on health and well-being.
Sleep deprivation is a more severe form of sleep loss...
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A Chronic Sleep Fragmentation Model using Vibrating Orbital Rotor to Induce Cognitive Deficit and Anxiety-Like Behavior in Young Wild-Type Mice
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Chronic sleep fragmentation induces endothelial dysfunction and structural vascular changes in mice.

Alba Carreras1, Shelley X Zhang1, Eduard Peris1

  • 1Section of Pediatric Sleep Medicine, Department of Pediatrics, Comer Children's Hospital, Pritzker School of Medicine, The University of Chicago, Chicago, IL.

Sleep
|November 4, 2014
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Summary

Long-term sleep fragmentation (SF) in mice impaired endothelial function and increased blood pressure. SF also caused vascular changes, including elastic fiber disruption and inflammation, suggesting a role in obstructive sleep apnea (OSA) cardiovascular risks.

Keywords:
atherosclerosiscell senescenceendothelial functionsleep apnea

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Area of Science:

  • Cardiovascular Science
  • Sleep Medicine
  • Vascular Biology

Background:

  • Sleep fragmentation (SF) is a hallmark of obstructive sleep apnea (OSA).
  • The direct link between SF and cardiovascular morbidities in OSA remains unclear.
  • Existing research suggests SF may contribute to OSA-related health issues.

Purpose of the Study:

  • To investigate the long-term effects of SF on vascular endothelial function and structure.
  • To determine if SF contributes to cardiovascular changes observed in OSA.
  • To test the hypothesis that SF leads to endothelial dysfunction and altered vessel wall structure.

Main Methods:

  • Adult male C57BL/6J mice were subjected to 20 weeks of controlled sleep fragmentation (SF) or normal sleep (CTL).
  • Weekly assessments included telemetric blood pressure monitoring and laser-Doppler assessment of endothelial function.
  • Aortic tissues were analyzed for atherosclerotic plaques, elastic fiber integrity, cellular infiltration (foam cells, macrophages), and senescence markers.

Main Results:

  • Mice exposed to SF exhibited delayed post-occlusive hyperemia and elevated blood pressure starting at 8 weeks.
  • SF induced significant elastic fiber disruption and disorganization in the aorta, alongside increased foam cells and macrophage infiltration.
  • Altered expression of senescence markers (reduced TERT and cyclin A, increased p16INK4a) and elevated plasma IL-6 were observed in SF mice.

Conclusions:

  • Chronic sleep fragmentation induces vascular endothelial dysfunction and mild hypertension.
  • SF leads to structural vascular changes, including elastic fiber damage and inflammation.
  • Findings support a role for SF in the cardiovascular complications associated with OSA.