Nathalie Loos

Sympathetic nervous control of the cerebral circulation in sleep

Cerebral vessels are extensively innervated by sympathetic nerves arising from superior cervical ganglia, and these nerves might play a protective role during the large arterial pressure surges of active sleep (AS). We studied lambs (n = 10) undergoing spontaneous sleep–wake cycles before and after bilateral removal of the superior cervical ganglia (SCGx, n = 5) or sham ganglionectomy (n = 5). Lambs were instrumented to record cerebral blood flow (CBF, flow probe on the superior sagittal sinus), carotid arterial pressure (Pca), intra‐cranial pressure (Pic), cerebral perfusion pressure (Pcp = Pca−Pic) and cerebral vascular resistance (CVR). Prior to SCGx, CBF (mL min−1) was significantly higher in AS than in Quiet Sleep (QS) and Quiet Wakefulness (QW) (17 ± 2, 13 ± 3, and 14 ± 3 respectively, mean ± SD, P < 0.05). Following SCGx, baseline CBF increased by 34, 31, and 29% respectively (P < 0.05). CVR also decreased in all states by ∼25% (P < 0.05). During phasic AS, surges of Pca were associated with transient increases in Pcp, Pic and CBF. Following SCGx, peak CBF and Pic during surges became higher and more prolonged (P < 0.05). Our study is the first to reveal that tonic sympathetic nerve activity (SNA) constricts the cerebral circulation and restrains baseline CBF in sleep. SNA is further incremented during arterial pressure surges of AS, limiting rises in CBF and Pic, possibly by opposing vascular distension as well as by constricting resistance vessels. Thus, SNA may protect cerebral microvessels from excessive distension during AS, when large arterial blood pressure surges are common.

Spontaneous motor activity in fat-fed, streptozotocin-treated rats: a nonobese model of type 2 diabetes.

We investigated the effects of diabetes on the spontaneous motor activities (SMA) of streptozotocin-treated rats fed a high-fat diet (HFD), a new nonobese model of type 2 diabetes. The daily changes in the duration of SMA were assessed via infrared cells, which detected all movements of rats that had been fed for 3 weeks with a standard or HFD and then injected with vehicle or 50 mg/kg of streptozotocin. Five to six days after streptozotocin injection, the daily body weight and the levels of duration of SMA of the diabetic rats were depressed, manifest by a substantial decline in the frequency of occurrence of nocturnal SMA episodes. The dramatic depression of daily duration of SMA levels observed in the rats given a HFD and treated with streptozotocin appears to be related solely to the diabetic state and not to body weight and/or HFD consumption, since the HFD (and/or related metabolic effects) remained ineffective in altering this feature in rats that grow normally. By thoroughly separating the prediabetic and the diabetic phases, we have been able to more readily explore the deleterious effects of the stages of both of these phases on changes in daily SMA levels.

Effect of high-fat diet and metformin treatment on ventilation and sleep apnea in non-obese rats.

We investigated the effect of insulin resistance on ventilation and the incidence of sleep apnea in non-obese rats and determined whether metformin could change ventilation and occurrence of sleep apneas. Five groups of rats were studied: (1) standard chow; (2) high-fat groups, with 1 with metformin; (2) had type 2 diabetes induced by streptozotocin, with 1 with metformin. Compared to standard rats, ventilatory parameters remained unchanged in the high-fat fed diet as well as in diabetic rats. However, their oxygen consumption was reduced (p<or=0.01). They had a lower ventilatory response to CO2 challenge (p<or=0.01), and their sleep apnea scores increased markedly (p<or=0.001). These results suggest that insulin resistance could impair the ventilation control. Metformin treatment, known to reduce insulin resistance, got sleep apnea scores back to their basic levels, reinforcing the idea that insulin resistance is a major factor in the occurrence of apneas in this rat model.

Effects of GSM 900 MHz on Middle Cerebral Artery Blood Flow Assessed by Transcranial Doppler Sonography

Mobile phone use has increased worldwide but its possible effects on the brain remain unclear. The aim of the present study was to investigate the effect of acute exposure to a radio frequency electromagnetic field (RF EMF) generated by a mobile phone operating in the Global System for Mobile Communication (GSM) 900 MHz on cerebral blood flow. Twenty-nine volunteers attended two experimental sessions: a sham exposure session and a real exposure session in a cross-over double-blind study in which a mobile phone was positioned on the left side of the head. In one session, the mobile phone was operated without RF radiation (sham phone) and in the other study it was operated with RF radiation (real phone) for 20 min. Thus, each subject served as its own control. Middle cerebral artery blood flow was monitored noninvasively by transcranial Doppler sonography to measure middle cerebral artery blood flow velocity. Pulsatility index and resistance index were also evaluated. A voluntary breath holding physiological test was carried out as a positive control for testing cerebral vasoreactivity. Hemodynamic variables were recorded and analyzed before, during and after mobile phone exposure. No significant changes were detected in studied variables in middle cerebral arteries during sham or real exposure. In the exposed side the cerebral blood flow velocity, the pulsatility index and the resistance index during sham and real exposure were respectively: [61.9 ± 1.3, 61.7 ± 1.3 cm/s (P = 0.89)]; [0.93 ± 0.03, 0.90 ± 0.02 (P = 0.84)] and [0.58 ± 0.01, 0.58 ± 0.01 (P = 0.96)] at baseline; and [60.6 ± 1.3, 62 ± 1.6 cm/s (P = 0.40)]; [0.91 ± 0.03, 0.87 ± 0.03 (P = 0.97)]; [0.57 ± 0.01, 0.56 ± 0.01 (P = 0.82)] after 20 min of exposure. Twenty minutes of RF exposure to a mobile phone does not seem to affect the cerebral circulation.

Is the Effect of Mobile Phone Radiofrequency Waves on Human Skin Perfusion Non-Thermal?

To establish whether SkBF can be modified by exposure to the radiofrequency waves emitted by a mobile phone when the latter is held against the jaw and ear.

Sleep structure and feeding pattern changes induced by the liver's thermal status in the rat.

Given the liver’s importance in controlling metabolic homeostasis in mammals, we sought to establish (i) whether the thermal status of this organ was involved in the link between sleep, thermoregulation and food intake and (ii) how the hypothalamic structures affect the functional interactions between processes involved in regulation of the body’s energy balance. In 10 freely moving rats, the liver was heated artificially to and maintained at set‐point temperatures of 39.5, 40.0 and 40.5 °C for 4 h. Each animal’s feeding activity, cortical temperature and brown adipose tissue (TBAT) temperature were measured continuously. Sleep organization and wakefulness were scored from electroencephalograms. Each animal served as its own control. Heating the liver induced a decrease in food intake and TBAT, corresponding to the development of a hypometabolic hypothermic status. The total amounts of wakefulness and rapid eye movement sleep fell, whereas the total amount of slow wave sleep increased accordingly. Our findings show that the liver is involved significantly in the body’s thermodynamic equilibrium. The organ’s thermal status can induce well‐coordinated behavioural and autonomic adaptive responses involved in the control of food intake and in the maintenance of body homeothermia. Our study provides indirect evidence of the existence of hepatic thermosensors afferent to feeding and sleeping hypothalamic integrating centres that can be stimulated by physiological increases in liver temperature.

Does Exposure to a Radiofrequency Electromagnetic Field Modify Thermal Preference in Juvenile Rats

Some studies have shown that people living near a mobile phone base station may report sleep disturbances and discomfort. Using a rat model, we have previously shown that chronic exposure to a low-intensity radiofrequency electromagnetic field (RF-EMF) was associated with paradoxical sleep (PS) fragmentation and greater vasomotor tone in the tail. Here, we sought to establish whether sleep disturbances might result from the disturbance of thermoregulatory processes by a RF-EMF. We recorded thermal preference and sleep stage distribution in 18 young male Wistar rats. Nine animals were exposed to a low-intensity RF-EMF (900 MHz, 1 V.m−1) for five weeks and nine served as non-exposed controls. Thermal preference was assessed in an experimental chamber comprising three interconnected compartments, in which the air temperatures (Ta) were set to 24°C, 28°C and 31°C. Sleep and tail skin temperature were also recorded. Our results indicated that relative to control group, exposure to RF-EMF at 31°C was associated with a significantly lower tail skin temperature (−1.6°C) which confirmed previous data. During the light period, the exposed group preferred to sleep at Ta = 31°C and the controls preferred Ta = 28°C. The mean sleep duration in exposed group was significantly greater (by 15.5%) than in control group (due in turn to a significantly greater amount of slow wave sleep (SWS, +14.6%). Similarly, frequency of SWS was greater in exposed group (by 4.9 episodes.h−1). The PS did not differ significantly between the two groups. During the dark period, there were no significant intergroup differences. We conclude that RF-EMF exposure induced a shift in thermal preference towards higher temperatures. The shift in preferred temperature might result from a cold thermal sensation. The change in sleep stage distribution may involve signals from thermoreceptors in the skin. Modulation of SWS may be a protective adaptation in response to RF-EMF exposure.