PubMed Health⌕ Search

Biomedical subjects

A Buguet

Publications and source records attributed to A Buguet.

At least 37 records · Page 2Linked to original sources
PubMed2000

Effects of zopiclone on the rest/activity rhythm after a westward flight across five time zones.

The effects of zopiclone on the rest/activity rhythm were investigated after a westward flight with a 5-h phase delay (Grenoble-Martinique). The rest/activity rhythm was recorded continuously with an actigraph monitor during a 6-day baseline episode in Grenoble and a 6-day sojourn in Martinique. Rectal temperature was recorded before the flight on day 2 and after the flight on days 2 and 5. Subjective jet-lag score was assessed before the flight on days 1 and 2 and in Martinique on days 1, 2, 5 and 6. Zopiclone (7.5 mg) or placebo were administered double blind 30 min prior to bedtime during the first 4 post-flight days (D1-D4). Under zopiclone treatment, sleep was less fragmented on the first post-flight night and the curtailment of sleep duration observed on D2 and D3 under placebo was prevented. During day-time, subjects tended to be more active than with placebo. By contrast, subjective jet-lag scores did not differ between both groups. Zopiclone seemed to accelerate the readjustment of the rest/activity rhythm and the normalisation of the phase relationship between sleep and the temperature rhythm. Zopiclone probably exerts its "resetting" effects on jet-lag desynchronosis by facilitating sleep induction rather than via a chronobiotic action.

Analysis of Variance↗
PubMed2000

L-Arginine availability modulates local nitric oxide production and parasite killing in experimental trypanosomiasis.

Nitric oxide (NO) is an important effector molecule of the immune system in eliminating numerous pathogens. Peritoneal macrophages from Trypanosoma brucei brucei-infected mice express type II NO synthase (NOS-II), produce NO, and kill parasites in the presence of L-arginine in vitro. Nevertheless, parasites proliferate in the vicinity of these macrophages in vivo. The present study shows that L-arginine availability modulates NO production. Trypanosomes use L-arginine for polyamine synthesis, required for DNA and trypanothione synthesis. Moreover, arginase activity is up-regulated in macrophages from infected mice from the first days of infection. Arginase competes with NOS-II for their common substrate, L-arginine. In vitro, arginase inhibitors decreased urea production, increased macrophage nitrite production, and restored trypanosome killing. In vivo, a dramatic decrease in L-arginine concentration was observed in plasma from infected mice. In situ restoration of NO production and trypanosome killing were observed when excess L-arginine, but not D-arginine or L-arginine plus N(omega)-nitro-L-arginine (a NOS inhibitor), was injected into the peritoneum of infected mice. These data indicate the role of L-arginine depletion, induced by arginase and parasites, in modulating the L-arginine-NO pathway under pathophysiological conditions.

Animals↗
PubMed1999

Reversal of the sleep/wake cycle disorder of sleeping sickness after trypanosomicide treatment.

To determine whether the circadian disruption of the sleep/wake cycle observed in sleeping sickness, human African trypanosomiasis (HAT), can be reversed after trypanosomicide treatment, 10 Congolese patients infected by Trypanosoma brucei gambiense underwent 24-h polysomnographic recordings before treatment with melarsoprol and after each of three weekly treatment sessions. Polysomnography consisted of a continuous recording of the electroencephalogram, electromyogram and electro-oculogram on a Minidix Alvar polygraph. Sleep traces were analysed in 20-sec epochs for wakefulness, REM sleep, and NREM sleep [stages 1, 2, 3, 4; stages 3 and 4 representing slow-wave sleep (SWS)]. As previously described (Buguet et al. 1993), the 24-h distribution of the sleep/wake cycle was disturbed proportionally to the severity of the illness. The overall amounts of each sleep/wake stage did not change after treatment. However, the patterns of occurrence of sleep episodes, REM sleep and SWS phases were determinant in the evaluation of treatment efficacy. The trypanosomicide action of melarsoprol led to a reduction in the number of sleep episodes, except in one patient whose health condition worsened during the third treatment session: sleep onset REM sleep phases (SOREMPs) decreased and the number of SWS episodes during a sleep episode increased. We conclude that in HAT, the reversibility of the sleep/wake cycle alteration and that of sleep structure constitute the basis for an evaluation of the healing process.

Adult↗
PubMed1999

Voltammetric measurement of blood nitric oxide in irradiated rats.

UNLABELLED: PURPOSE. To investigate the effect of blood nitric oxide (NO) as a mediator of the neurovascular syndrome in rats following gamma-irradiation. MATERIAL AND METHODS: Using a voltametric method together with a carbon fibre based sensor, NO measurements were carried out in sham-irradiated and irradiated animals either in blood from the abdominal aorta or in blood samples from the heart. RESULTS: In in vitro conditions, properties of the probe were not altered by the ionizing radiation. Significant increases of +17% and +25.6% were observed in the voltametric signal height at 90 min and 24 h respectively after a 15 Gy gamma-ray exposure. These effects were followed on days 3 and 4 by a progressive decrease in the signal height of 7% and 18% respectively. Dose-effect relationships were observed at 90 min and 24 h after exposure to gamma-rays in the range of 3-15 Gy. Finally, the NO dependence on the measured voltametric signal was controlled by using inhibitors of the NO synthase (NOS) and by performing nitrate assays. CONCLUSIONS: Specific blood NO voltametric measurements are possible. Functional changes associated with NO after gamma-ray exposure are discussed.

Animals↗
PubMed1999

Contribution of exertional hyperthermia to sympathoadrenal-mediated lymphocyte subset redistribution.

The contribution of hyperthermia to the differential leukocytosis of exercise remains obscure. This study examined changes in circulating sympathoadrenal hormone concentrations and patterns of leukocyte and lymphocyte subset (CD3(+), CD4(+), CD8(+), CD19(+), CD3(-)16(+)/56(+)) redistribution during exercise, with and without a significant rise of rectal temperature (T(re)). Ten healthy men [age 26.9 +/- 5.7 (SD) yr, body mass 76.0 +/- 10.9 kg, body fat 13.9 +/- 4.6%, peak O(2) consumption: 48.0 +/- 12.4 ml x kg(-1) x min(-1)] exercised for 40 min (65% peak O(2) consumption) during water immersion at 39 or 18 degrees C. T(re) increased from 37.2 to 39.3 degrees C (P < 0.0001) after 40 min of exercise in 39 degrees C water but was held constant to an increment of 0.5 degrees C during exercise in 18 degrees C water. Application of this thermal clamp reduced exercise-associated increments of plasma epinephrine (Epi) and norepinephrine (NE) by >50% (P < 0.05) and abolished the postexercise increase in cortisol. Thermal clamping also reduced the exercise-induced leukocytosis and lymphocytosis. Multiple regression demonstrated that T(re) had no direct association with lymphocyte subset mobilization but was significantly (P < 0.0001) correlated with hormone levels. Epi was an important determinant of total leukocytes, lymphocytes, and CD3(+), CD4(+), CD8(+), and CD3(-)CD16(+)/56(+) subset redistribution. The relationship between NE and lymphocyte subsets was weaker than that with Epi, with the exception of CD3(-)CD16(+)/56(+) counts, which were positively (P < 0.0001) related to NE. Cortisol was negatively associated with leukocytes, CD14(+) monocytes, and CD19(+) B- and CD4(+) T-cell subsets but was positively related to granulocytes. We conclude that hyperthermia mediates exercise-induced immune cell redistribution to the extent that it causes sympathoadrenal activation, with alterations in circulating Epi, NE, and cortisol.

Adrenal Glands↗
PubMed1999

Is sleeping sickness a circadian disorder? The serotonergic hypothesis.

Patients with human African trypanosomiasis (HAT, sleeping sickness), due to the inoculation of Trypanosoma brucei gambiense or rhodesiense by the tsetse fly, are "sleepy by day and restless by night." The first 24 h polysomnographic recording (electroencephalogram [EEG], electromyogram [EMG], electrooculogram [EOG]), showing a disappearance of the 24 h rhythmicity of sleep and wakefulness, was performed in 1988. Thereafter, our team recorded 18 patients and 6 control volunteers at bed rest during 24 h sessions. Blood samples were taken hourly from 8 of the patients through a venous catheter and every 10 minutes from the remaining 10 patients. Plasma cortisol, prolactin, growth hormone (GH), melatonin, and plasma renin activity were analyzed. No disruptions of the circadian rhythms of sleep and wakefulness were described in the 6 healthy African subjects, and there also were no disturbances of 24 h hormone profiles. The patients experienced a dysregulation of the circadian rhythmicity of sleep and wakefulness that was proportional to the severity of the disease. Sleep onset rapid eye movement (REM) episodes were more frequent in the most severely sick patients, who also showed major disruptions in the 24 h plasma hormonal profiles, with intermediate profiles being observed at earlier stages of the sickness. However, the relationship between hormonal secretions and the states of vigilance persisted. Contrary to the other hormones, melatonin secretion remained undisturbed. These findings indicate that, at the stage of meningoencephalitis, HAT represents a dysregulation of the sleep-wake cycle and sleep structure, rather than a hypersomnia; this dysregulation is proportional to the degree of severity of the clinical and biological symptoms. It is accompanied by a circadian dysrhythmia of hormonal secretions, although the relationship between hormone pulses and sleep states is preserved. We therefore favor the involvement of the serotonergic raphe nuclei-suprachiasmatic nuclei liaison in the reversible disturbance of the circadian rhythms of the sleep-wake cycle and of hormonal secretions.

Animals↗
PubMed1998

Exercise-induced hyperthermia and hormonal responses to exercise.

Changes in plasma hormonal concentrations during exercise have been ascribed to the type, duration, and intensity of exercise, physical fitness of subjects, oxygen availability and debt, and acid-base balance. However, relatively few studies have examined the possible role of exercise-induced hyperthermia. This paper reviews previous studies on this subject and describes a series of experiments carried out in our laboratories to define the role of changes in body temperature in the release of hormones during exercise. In a first series of experiments, we studied the relationship between thermoregulatory and growth hormone responses to severe exercise at 23 degrees C for 2 h in fit euhydrated subjects, controlling the core temperature increase to a maximum of 40 degrees C by varying wind speed. Exponential relationships were found between increases in core temperature and plasma growth hormone, prolactin, and catecholamines during exercise, suggesting the existence of a thermal threshold for stimulation of hormonal release during exercise. The effect of endurance exercise with and without a thermal clamp (immersion in cold and warm water) on hormonal and leukocyte responses was examined. Again, a significant exponential relationship was found between increases in core temperature and hormonal responses. Thermal clamping significantly diminished the hormonal and the leukocytic responses to exercise, suggesting that an exercise-induced thermal threshold of approximately 38 degrees C exists where hormonal responses are observed. Therefore, core temperature increases may be integrated in the controlling system of hormonal and leukocytic responses to exercise.

Body Temperature↗
PubMed1998

Sleep and stress in man: an approach through exercise and exposure to extreme environments.

In this paper, the effects of exercise on human sleep (in temperate, cold, and hot climates) are compared with those of exposure to extreme environments (tropical, polar climates). Exercise has two effect: (i) when the exercise load is too heavy or if the subject is not trained to the exercise conditions, the hypothalamo-pituitary-adrenocortical axis (HPA) is strongly activated (somatic stress reaction), and a diachronic (delayed) decrease in total sleep time and slow-wave sleep (SWS) occurs with a synchronic (concomitant) sleep disruption (such as a decrease in REM sleep); (ii) a diachronic enhancement of SWS and (or) REM sleep occurs during moderate training and in athletes, with a moderate HPA activation (neurogenic stress reaction). Heat acclimatization (neurogenic stress response) results in a diachronic increase in SWS, contrary to acute heat exposure (somatic stress) which leads to a diachronic decrease in SWS. Nocturnal cold exposure (somatic and (or) neurogenic stress) provokes a synchronic decrease in REM sleep with an activation of stress hormones, which are reduced by previous acclimation (neurogenic pathway); SWS remains undisturbed in the cold, as it occurs at the beginning of the night before body cooling. In conclusion, when the brain can deal with the stressor (neurogenic stress), diachronic increases in SWS and (or) REM sleep occur. When these "central" mechanisms are overloaded, the classical "somatic" stress reaction occurs with diachronic and synchronic disruptions of the sleep structure.

Acclimatization↗
PubMed1998

Plasma melatonin rhythm is maintained in human African trypanosomiasis.

In human African trypanosomiasis (sleeping sickness), sleep and wake episodes are sporadically distributed throughout the day and the night. Plasma melatonin, sleep-wakefulness and rectal temperature rhythms were studied in 9 Congolese patients suffering from sleeping sickness compared to 6 healthy controls submitted to the same light/dark regime. The circadian distribution of the sleep-wake cycle was disturbed in relation to the severity of the disease. As controls, patients maintained a very distinct plasma melatonin nyctohemeral rhythm which displayed a significant phase advance (1:08 +/- 0:43 and 2:34 +/- 0:31 mean +/- SD, in patients and controls respectively; p < 0.01, U test), as well as a persistent rectal temperature rhythm (mesor 36.67 +/- 0.29 and 36.74 +/- 0.13 degrees C, amplitude 0.29 +/- 0.16 and 0.32 +/- 0.13 degrees C, acrophase 13:53 +/- 2:47 and 15:32 +/- 0:36 for patients and controls respectively). No alteration of these rhythms was observed after treatment. In African controls we observed plasma melatonin characteristics similar to those of European controls, especially for the onset and the duration of the secretion and the stability of the rhythm, despite a different light/dark regime. The dissociation observed between the 3 rhythms (melatonin, temperature and sleep-wake cycle) is discussed, taking into consideration a functional compartmentalization of the suprachiasmatic nuclei or more likely a disruption of the neural pathway between the circadian clock and structures involved in the regulation of the sleep-wake cycle, related to the activity of compounds released by the parasites or host cells.

Adolescent↗
PubMed1997

Voltametric assessment of brain nitric oxide during heatstroke in rats.

Anesthetized rats exposed to a high ambient temperature develop heatstroke with brain ischemia. Since nitric oxide (NO) plays an important role during normothermic ischemia, its cortical and cerebellar production were continuously assessed in pentobarbital anesthetized rats exposed to heat by using differential pulsed voltammetry. After 60 min at thermoneutrality, the rats were submitted to an ambient temperature of 40 degrees C until death. After 60 min in the heat, the rats were injected intraperitoneally with saline, MK801 (1 mg.kg(-1)), an antagonist of N-methyl-D-aspartate (NMDA) receptors, or L-arginine p-nitroanilide (L-ANA; 100 mg.kg(-1)), an inhibitor of NO synthase. Just before death, a 70% increase in NO production was observed in both the cerebellum and the cortex of saline-treated rats. The cortical increase in NO was not modified by MK801 while the NO signal was suppressed by L-ANA.

Animals↗
PubMed1997

Effect of melarsoprol treatment on circulating IL-10 and TNF-alpha levels in human African trypanosomiasis.

The pathogenesis of human African trypanosomiasis (HAT) has been the object of considerable research interest but has remained incompletely understood. The importance of cytokines in the pathophysiology of this protozoan infection is now widely recognized, but the full spectrum of cytokines involved has yet to be determined. In the present investigation we compared the plasma concentrations of TNF-alpha and IL-10 in normal African controls and patients suffering from advanced meningocephalic (late-stage) Trypanosomiasis brucei (T.b.) gambiense infections, before and after treatment with the arsenical trypanocide melarsoprol. We found that patients with late-stage T. b. gambiense exhibit chronically elevated circulating levels of both of these cytokines, and that these levels quickly decline following melarsoprol treatment. These findings confirm that TNF-alpha is involved in the immunopathogenesis of late-stage African trypanosomiasis and suggest that IL-10 may also play an important regulatory role in this disease.

Adolescent↗
PubMed1996

Electroencephalographic and polygraphic features of 24-hour recordings in sleeping sickness and healthy African subjects.

Electroencephalographic (EEG) and polygraphic features were analysed in six healthy control subjects and eight patients suffering from sleeping sickness meningoencephalitis in order to determine possible functional relationships. One patient was disqualified because of intermittent metabolic disease. Twenty-four h polygraphic recordings-EEG, electrooculography (EOG), electromyography (EMG), nasal and buccal air flow, chest respiratory movements-were performed continuously both on paper and on cassette tapes. Tapes were played back on paper (paper speed: 15 mm/s). Traces were analyzed for normal and pathologic features, and transient activation phases and paroxysmal hypnopompic hypersynchrony events were counted. During wakefulness, slow theta and delta waves occurred in four patients, but alpha reactivity was present. During sleep, normal features were seen. However, transient activation phases were decreased in the patients. During slow-wave sleep, four patients presented predominantly monophasic frontal delta bursts along with paroxysmal hypnopompic hypersynchrony events. In conclusion, in sleeping sickness patients, although dampened, the waking process remains responsive and slows down only during the late stage of meningoencephalitis.

Adolescent↗
PubMed1996

Relationship of plasma growth hormone to slow-wave sleep in African sleeping sickness.

Human African trypanosomiasis (sleeping sickness) is a unique disease model of disrupted circadian rhythms in the sleep-wake cycle and cortisol and prolactin secretion. This study examined the temporal relationship between growth hormone (GH) secretion and the sleep-wake cycle in 8 infected African patients and 6 healthy indigenous African subjects. Twenty-four-hour sleep patterns were recorded by polysomnography and hourly blood samples analyzed for plasma GH. No relationships between the mean normalized plasma GH levels (Z scores) and the sleep stages (wakefulness, sleep stages 1 and 2 ('light' sleep), slow-wave sleep (stages 3 and 4, SWS), and rapid eye movement (REM) sleep) were found in the patients or healthy subjects. However, when the time of sampling of the plasma GH concentrations was lagged by 16 min with respect to the occurrence of the various sleep stages, significant correlations were found between plasma GH concentrations and SWS in both healthy subjects and patients. Thus, the association between SWS and GH secretion persisted even in the presence of disrupted circadian rhythms, further supporting the concept that sleep and the stimulation of GH secretion are outputs of a common mechanism.

Adolescent↗
PubMed1996

Disruption of endocrine rhythms in sleeping sickness with preserved relationship between hormonal pulsatility and the REM-NREM sleep cycles.

In human African trypanosomiasis (sleeping sickness), sleep and wake episodes are sporadically distributed throughout the day and the night. To determine whether these sleep disturbances affect the 24-h hormone profiles and the normal relationships between hormone pulsatility and sleep stages, polygraphic sleep recordings and concomitant hormone profiles were obtained in 6 African patients with sleeping sickness and in 5 healthy African subjects selected from Abidjan on the Ivory Coast. Polysomnographic recordings were continuous, and blood was taken every 10 min throughout the 24-h period. Plasma was analyzed for cortisol, prolactin, and plasma renin activity (PRA). The 24-h rhythm of cortisol, considered to be an endogenous circadian rhythm, was attenuated in all of the patients except one. However, as in normal subjects, slow wave sleep (SWS) remained associated with the declining phases of the cortisol secretory episodes. Prolactin and PRA profiles, which are strongly influenced by the sleep-wake cycle, did not manifest the nocturnal increase normally associated with the sleep period; instead, they reflected a sporadic distribution of the sleep and wake episodes throughout the 24-h period. In patients with sleeping sickness as in normal subjects, rapid eye movement (REM) sleep began during the descending phases of prolactin pulses. In both groups, PRA reflected the sleep stage distribution with non REM (NREM) sleep occurring during the ascending phases and REM sleep during the descending phases of the PRA oscillations. However, in sleeping sickness patients, the marked sleep fragmentation often did not allow sufficient time for PRA to increase significantly, as is normally the case in subjects with regular NREM-REM sleep cycles. These results demonstrate that, together with the disruption of the sleep-wake cycle, there are profound differences in the temporal organization of the 24-h hormone profiles in humans with African trypanosomiasis. However, the relationship between hormonal pulses and specific sleep stages persists, indicating the existence of a robust link between hormonal release and the internal sleep structure.

Adult↗
PubMed1996

[Action duality of nitrogen oxide (NO) in experimental African trypanosomiasis].

Patients with human African trypanosomiasis present a major dysruption of the circadian rhythmicity of the sleep-wake cycle, which was also found in rats infected with Trypanosoma brucei brucei (T.b.b.). The alterations in the immune function and nervous system in African trypsanosomiasis led us to investigate the involvement of nitric oxide (NO), a key molecule in immune and neurophysiological mechanisms, in experimental trypanosomiasis. NO was measured in 35 Sprague Dawley rats using differential impulsional voltammetry with a carbon fiber coated with porphyrin-nickel and nafion, ex vivo in the blood and in vivo in the brain. The rats were anaesthetized with sodium chlorate. Infection was performed intraperitoneally (i.p.) with 0.2 ml of a T.b.b. cryostabilate (clone AnTat 1.1E). Blood was collected by an intracardiac puncture with immediate replacement of blood volume (1 ml) in 7 control rats and 8 rats infected since 15 days, before and after i.p. administration of L-ANA (L-arginine-p-nitro-anilide, 100 mg.kg-1, an inhibitor of NO synthase). Brain measures were done in 20 rats (8 controls, and 12 rats infected since 15 or 21 days), in the cortex (H, -0.5 mm; AP, -0.8 mm; L, 1.2 mm) and the lateral ventricle (H,-3.2 mm). In infected rats, blood NO was at 70% of control values (p < 0.001), and L-ANA suppressed the NO signal in all animals (p < 0.0001), demonstrating that the signal originated from NO. Cortical NO was higher than in the ventricle in both control (p < 0.0001) and infected rats (p < 0.001). NO was more elevated in both structures in 15-day-infected rats than in control rats (p < 0.0001), the difference being enhanced in 21-day-infected rats (p < 0.001). L-ANA suppressed the NO signal in 30 to 60 min. These data suggest that NO intervenes in the development of trypanosomiasis in different manners. It is increased in the brain, which remains unexplained, where it may be involved in blood-brain barrier permeation. Conversely, it is decreased in the blood, may be because of macrophage function impairment, which would explain why trypanosomes can multiply in the host.

Animals↗
PubMed1995

Twenty-four-hour profiles and sleep-related variations of cortisol, thyrotropin and plasma renin activity in healthy African melanoids.

The 24-h hormone profiles have been well documented in caucasians living in a temperate climate, but they have never been examined in melanoid subjects under equatorial conditions, with a 12-h light-dark cycle in a hot climate. To establish normal data for this population, blood samples were taken at 10-min intervals over 24 h in five healthy young melanoids living in Abidjan (Ivory Coast). Cortisol and thyroid stimulating hormone (TSH) concentrations and plasma renin activity (PRA) were determined by radio-immunoassay and sleep was registered using polysomnography. Data were compared with results obtained in Strasbourg (France) from six healthy aged-matched caucasians. The 24-h profile of cortisol concentration was similar in both groups, with a 2-h phase advance in the melanoids. Nocturnal fluctuations of PRA, strongly linked to the rapid eye movement-non rapid eye movement (REM-NREM) sleep cycles, occurred in both groups, with higher levels in the caucasians in the last 2 h of sleep along with greater amounts of NREM sleep. After an evening increase in TSH, the sleep onset-related decrease seen in the caucasians was not observed in the melanoids. In both groups, increasing concentrations of TSH and cortisol occurred with awakening, decreasing concentrations being observed during slow-wave sleep. As in the caucasians studied in the temperate climates, the melanoid subjects living at the equator showed the same temporal organization of hormone rhythms within the 24-h period and the same relationships between the pulses and specific sleep stages.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

[Continuous nocturnal automassage of an acupuncture point modifies sleep in healthy subjects].

To test the somnogenic properties of the automassage of point 7 heart of acupuncture, polygraphic night sleep was studied in six healthy volunteers (age: 27.8 +/- 1.6 years) from 23:00 h to 07:00 h. After one night of adaptation, two PEBA cones (Polyether Block Amides; Isocones) were fixed bilaterally at both points 7 heart (active application, AA) or on the back of hand (placebo application, AP). The alternate application was used 2 weeks later, using a randomized, double-blind, and cross-over protocol. Cyclic alternating patterns (CAP) were also analysed on the electroencephalogram during non-REM sleep. Sleep efficiency increased in AA, due to a decrease in wakefulness, and an increase in total sleep time due to an increase in non-REM sleep. The number of CAP decreased in AA, as did the number of CAP sequences and the ratio of CAP duration to total sleep time (CAP rate) and to the duration of slow-wave sleep. In conclusion, the application of Isocones at point 7 heart during the night induced a decrease in wakefulness and an increase in non-REM sleep during night sleep in healthy subjects.

Acupuncture Points↗