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

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

Surface Properties and Physicochemical Characterizations of a New Type of Anode Material, La_1−<i>x</i>Sr_<i>x</i>Cr_1−<i>y</i>Ru_<i>y</i>O_3−δ, for a Solid Oxide Fuel Cell under Methane at Intermediate Temperature

International audienceIn order to develop a new anodic material for a solid oxide fuel cell (SOFC) operated under methane, we studied lanthanum chromites doped with strontium and ruthenium. Ruthenium is an excellent catalyst for methane steam reforming but its use is limited by its cost and evaporation as RuOx at high temperature. To stabilize the ruthenium, we inserted it into the perovskite to form La1−xSrxCr1−yRuyO3. XRD, SEM, TPR, and EDX analyses revealed the stability of ruthenium in the perovskite, in the tetravalent state. The composition was homogeneous in the entire volume of the electrode. Nevertheless, XPS analyses indicated a strontium segregation for a thickness lower than 5 nm. The EDX analyses also showed a strontium concentration gradient near the subsurface. The main result was that no loss of ruthenium was detected even after treatments under air at 1100°C. The strontium doping allows the stabilization of the ruthenium in the perovskite in the tetravalent state. </p

A study on the optimal length of actigraphic recording in narcolepsy type 1

Objective: The aim of the present study was to assess the optimal length of actigraphic recordings in patients with narcolepsy type 1. Methods: A secondary analysis was carried out with the previously collected data in eleven patients with narcolepsy type 1. Ten of the 11 patients were medicated at the time of actigraphic recording. Each patient originally wore an Actiwatch AW64 actigraph for at least 28 consecutive days. Overall, the patients were analyzed for 308 nights. Results: No significant differences were observed between the mean values of the 7-day and 14-day analyzed sets for the parameters sleep efficiency, fragmentation index, sleep onset latency, wake after sleep onset, and total sleep time. Conclusions: Our data suggest that 7 days of actigraphic recording could be sufficient for these patients. Significance: Our results for the optimal length of actigraphic recording could be useful for both physicians and patients