100 research outputs found
Total sleep deprivation alters endothelial function in rats: a nonsympathetic mechanism
STUDY OBJECTIVES: Sleep loss is suspected to induce endothelial dysfunction, a key factor in cardiovascular risk. We examined whether sympathetic activity is involved in the endothelial dysfunction caused by total sleep deprivation (TSD). DESIGN: TWO GROUPS: TSD (24-h wakefulness), using slowly rotating wheels, and wheel control (WC). PARTICIPANTS: Seven-month-old male Wistar rats. INTERVENTIONS: Pharmacological sympathectomy (reserpine, 5 mg/kg, intraperitoneal), nitric oxide synthase (NOS) inhibition (N (G)-nitro-L-arginine, 20 mg/kg, intraperitoneally 30 min before experiment) and cyclooxygenase (COX) inhibition (indomethacin, 5 mg/kg, intraperitoneally 30 min before experiment). MEASUREMENTS AND RESULTS: In protocol 1, changes in heart rate (HR) and blood pressure were continuously recorded in the sympathectomized and non-sympathectomized rats. Blood pressure and HR increased during TSD in non-sympathectomized rats. In protocol 2, changes in skin blood flow (vasodilation) were assessed in the sympathectomized and non-sympathectomized rats using laser-Doppler flowmetry coupled with iontophoretic delivery of acetylcholine (ACh), sodium nitroprusside (SNP), and anodal and cathodal currents. ACh- and cathodal current-induced vasodilations were significantly attenuated after TSD in non-sympathectomized and sympathectomized rats (51% and 60%, respectively). In protocol 3, ACh-induced vasodilation was attenuated after NOS and COX inhibition (66% and 49%, respectively). Cathodal current-induced vasodilation decreased by 40% after COX inhibition. In TSD compared to WC a decrease in ACh-induced vasodilation was still observed after COX inhibition. No changes in SNP- and anodal current-induced vasodilation were detected. CONCLUSION: These results demonstrate that total sleep deprivation induces a reduction in endothelial-dependent vasodilation. This endothelial dysfunction is independent of blood pressure and sympathetic activity but associated with nitric oxide synthase and cyclooxygenase pathway alterations
Effect of acute sleep deprivation on vascular function in healthy subjects
Sleep disorders are associated with inflammation and sympathetic activation, which are suspected to induce endothelial dysfunction, a key factor in the increased risk of cardiovascular disease. Less is known about the early effects of acute sleep deprivation on vascular function. We evaluated microvascular reactivity and biological markers of endothelial activation during continuous 40 h of total sleep deprivation (TSD) in 12 healthy men (29 +/- 3 yr). The days before [day 1 (D1)] and during TSD (D3), at 1200 and 1800, endothelium-dependent and -independent cutaneous vascular conductance was assessed by iontophoresis of acetylcholine and sodium nitroprusside, respectively, coupled to laser-Doppler flowmetry. At 0900, 1200, 1500, and 1800, heart rate (HR) and instantaneous blood pressure (BP) were recorded in the supine position. At D1, D3, and the day after one night of sleep recovery (D4), markers of vascular endothelial cell activation, including soluble intercellular adhesion molecule-1, vascular cell adhesion molecule-1, E-selectin, and interleukin-6 were measured from blood samples at 0800. Compared with D1, plasma levels of E-selectin were raised at D3, whereas intercellular adhesion molecule-1 and interleukin-6 were raised at D4 (P < 0.05). The endothelium-dependent and -independent CVC were significantly decreased after 29 h of TSD (P < 0.05). By contrast, HR, systolic BP, and the normalized low-frequency component of HR variability (0.04-0.15 Hz), a marker of the sympathetic activity, increased significantly within 32 h of TSD (P < 0.05). In conclusion, acute exposure to 40 h of TSD appears to cause vascular dysfunction before the increase in sympathetic activity and systolic BP
Estimation and quantification of vigilance using ERPs and eye blink rate with a fuzzy model-based approach
Physiological and autonomic stress responses after prolonged sleep restriction and subsequent recovery sleep in healthy young men
Purpose Sleep restriction is increasingly common and associated with the development of health problems. We investigated how the neuroendocrine stress systems respond to prolonged sleep restriction and subsequent recovery sleep in healthy young men. Methods After two baseline (BL) nights of 8 h time in bed (TIB), TIB was restricted to 4 h per night for five nights (sleep restriction, SR, n = 15), followed by three recovery nights (REC) of 8 h TIB, representing a busy workweek and a recovery weekend. The control group (n = 8) had 8 h TIB throughout the experiment. A variety of autonomic cardiovascular parameters, together with salivary neuropeptide Y (NPY) and cortisol levels, were assessed. Results In the control group, none of the parameters changed. In the experimental group, heart rate increased from 60 +/- 1.8 beats per minute (bpm) at BL, to 63 +/- 1.1 bpm after SR and further to 65 +/- 1.8 bpm after REC. In addition, whole day low-frequency to-high frequency (LF/HF) power ratio of heart rate variability increased from 4.6 +/- 0.4 at BL to 6.0 +/- 0.6 after SR. Other parameters, including salivary NPY and cortisol levels, remained unaffected. Conclusions Increased heart rate and LF/HF power ratio are early signs of an increased sympathetic activity after prolonged sleep restriction. To reliably interpret the clinical significance of these early signs of physiological stress, a follow-up study would be needed to evaluate if the stress responses escalate and lead to more unfavourable reactions, such as elevated blood pressure and a subsequent elevated risk for cardiovascular health problems.Peer reviewe
Effects of exercise on brain and peripheral inflammatory biomarkers induced by total sleep deprivation in rats
Antimicrobial Siloxane Statistical and Graft Copolymers Substituted with t-Butylamine and t-Butylammonium Biocidal Functions
The mineralogy and petrology of I-type cosmic spherules: Implications for their sources, origins and identification in sedimentary rocks
I-type cosmic spherules are micrometeorites that formed by melting during atmospheric entry and consist mainly of iron oxides and FeNi metal. I-types are important because they can readily be recovered from sedimentary rocks allowing study of solar system events over geological time. We report the results of a study of the mineralogy and petrology of 88 I-type cosmic spherules recovered from Antarctica in order to evaluate how they formed and evolved during atmospheric entry, to constrain the nature of their precursors and to establish rigorous criteria by which they may be conclusively identified within sediments and sedimentary rocks. Two textural types of I-type cosmic spherule are recognised: (1) metal bead-bearing (MET) spherules dominated by Ni-poor (100 and suggest that metal from H-group ordinary, CM, CR and iron meteorites may form the majority of particles. Oxidation during entry heating increases in the series MET 80 wt% Ni comprising a particle mass fraction of <0.2. Non-equilibrium effects in the exchange of Ni between wüstite and metal, and magnetite and wüstite are suggested as proxies for the rate of oxidation and cooling rate respectively. Variations in magnetite and wüstite crystal sizes are also suggested to relate to cooling rate allowing relative entry angle of particles to be evaluated. The formation of secondary metal in the form of sub-micron Ni-rich or Pt-group nuggets and as symplectite with magnetite was also identified and suggested to occur largely due to the exsolution of metallic alloys during decomposition of non-stoichiometric wüstite. Weathering is restricted to replacement of metal by iron hydroxides. The following criteria are recommended for the conclusive identification of I-type spherules within sediments and sedimentary rocks: (i) spherical particle morphologies, (ii) dendritic crystal morphologies, (iii) the presence of wüstite and magnetite, (iv) Ni-bearing wüstite and magnetite, and (v) the presence of relict FeNi metal
Polycroconaines de benzobisthiazoles : polymères à faible GAP ?
Des polycroconaines de N,N'-didodécylbenzobisthiazole angulaire (I) et de N,N'-dipropylsulfonate benzobisthiazole centro-symétrique (II) ont été synthétisées par condensation de
Knoevenagel et caractérisées. La polycroconaine (I) est soluble en milieu organique, alors que la polycroconaine (II) est pratiquement insoluble tant en milieu organique qu'en milieu aqueux. La
comparaison des caractéristiques spectroscopiques visible-proche IR des matériaux avec celles des molécules modèles a permis de montrer que dans ces polymères la conjugaison est limitée
une unité? structurale, le véritable gap se situant des énergies supérieures à 0,85 eV
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