Key result
Sleep fragmentation suppresses REM sleep and impairs cerebral blood flow in young mice.
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Either hypertension or chronic insomnia is the risk factor of developing vascular dementia. Durative hypertension can induce vascular remodeling and is used for modeling small vessel disease in rodents. It remains undetermined if the combination of hypertension and sleep disturbance exacerbates vascular dysfunction or pathologies. Previously, we found chronic sleep fragmentation (SF) dampened cognition in young mice without disease predispositions. In the current study, we superimposed SF with hypertension modeling in young mice. Angiotensin II (AngII)-releasing osmotic mini pumps were subcutaneously implanted to generate persistent hypertension, while sham surgeries were performed as controls. Sleep fragmentation with repetitive arousals (10 s every 2 min) during light-on 12 h for consecutive 30 days, while mice undergoing normal sleep (NS) processes were set as controls. Sleep architectures, whisker-stimulated cerebral blood flow (CBF) changes, vascular responsiveness as well as vascular pathologies were compared among normal sleep plus sham (NS + sham), SF plus sham (SF + sham), normal sleep plus AngII (NS + AngII), and SF plus AngII (SF + AngII) groups. SF and hypertension both alter sleep structures, particularly suppressing REM sleep. SF no matter if combined with hypertension strongly suppressed whisker-stimulated CBF increase, suggesting the tight association with cognitive decline. Hypertension modeling sensitizes vascular responsiveness toward a vasoactive agent, Acetylcholine (ACh, 5 mg/ml, 10 μl) delivered via cisterna magna infusion, while SF exhibits a similar but much milder effect. None of the modeling above was sufficient to induce arterial or arteriole vascular remodeling, but SF or SF plus hypertension increased vascular network density constructed by all categories of cerebral vessels. The current study would potentially help understand the pathogenesis of vascular dementia, and the interconnection between sleep and vascular health.
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Yang et al. (2023) studied Hypertension and chronic sleep fragmentation (preclinical vascular dementia model). Sleep fragmentation (10 s arousals every 2 min during 12-h light phase) plus Angiotensin II-releasing osmotic mini pumps vs. Normal sleep plus sham surgery (NS + sham), SF + sham, and NS + AngII was evaluated on Sleep architectures, whisker-stimulated cerebral blood flow (CBF) changes, vascular responsiveness to Acetylcholine (5 mg/ml, 10 μl), and vascular pathologies. Sleep fragmentation (10 s every 2 min for 30 days) with or without AngII-induced hypertension suppressed REM sleep and whisker-stimulated cerebral blood flow in young mice.
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