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Biomedical subjects

M Follenius

Publications and source records attributed to M Follenius.

At least 37 records · Page 2Linked to original sources
PubMed1994

Clomipramine-induced sleep disturbance does not impair its prolactin-releasing action.

The present study was undertaken to examine the role of sleep disturbance, induced by clomipramine administration, on the secretory rate of prolactin (PRL) in addition to the direct drug effect. Two groups of supine subjects were studied under placebo-controlled conditions, one during the night, when sleeping (n = 7) and the other at daytime, when awake (n = 6). Each subject received a single 50 mg dose of clomipramine given orally 2 hours before blood collection. Plasma PRL concentrations were analysed at 10 min intervals and underlying secretory rates calculated by a deconvolution procedure. For both experiments the drug intake led to significant increases in PRL secretion, acting preferentially on tonic secretion as pulse amplitude and frequency did not differ significantly from corresponding control values. During the night clomipramine ingestion altered the complete sleep architecture in that it suppressed REM sleep and the sleep cycles and induced increased wakefulness. As the relative increase in PRL secretion expressed as a percentage of the mean did not significantly differ between the night and day time studies (46 +/- 19% vs 34 +/- 10%), it can be concluded that the observed sleep disturbance did not interfere with the drug action per se. The presence of REM sleep was shown not to be a determining factor either for secretory pulse amplitude and frequency, as, for both, mean nocturnal values were similar with and without prior clomipramine ingestion.

Administration, Oral↗
PubMed1994

Prolactin secretion and sleep.

To clarify the relationship between prolactin (PRL) secretion and sleep, three experimental procedures were employed and secretory rates were estimated from plasma levels using a deconvolution procedure. Eight healthy young men participated in two 24-hour studies, one using normal night sleep and one using delayed sleep, to determine the influence of sleep as a whole on the PRL rhythm. Another group of 24 subjects underwent a 1-night study to investigate the relationship between PRL secretion and the internal sleep structure. The influence of sleep quality was studied in two more groups of eight subjects. Secretory rates were calculated by deconvolution from plasma PRL measured at 10-minute intervals. Sleep was recorded polygraphically in all experiments. PRL secretory pulses occurred throughout the 24-hour cycle without significant variation in frequency, but with enhanced pulse amplitude for both night and day sleep periods. Sleep onset was rapidly followed by an increase in secretion, and awakenings coincided with an immediate offset of active secretion. Analyzing the association between secretory pulses and sleep stages demonstrated that PRL secretory rate is low at the time of rapid eye movement sleep onset. Sleep quality appeared not to affect the PRL secretory profile. These results confirmed that PRL secretion is enhanced during the whole sleep period, as inferred from plasma levels. Considering secretory pulses provides a precise determination of the temporal relations between PRL and sleep structure and demonstrates that occasionally poor sleep does not influence PRL secretion in normal humans.

Adult↗
PubMed1994

Slow oscillations of plasma glucose and insulin secretion rate are amplified during sleep in humans under continuous enteral nutrition.

Concomitant oscillations of plasma glucose and insulin secretion rate with a periodicity of about 80 minutes have been identified in normal humans. To determine whether these slow oscillations are influenced by sleep, peripheral levels of glucose and C-peptide were measured at 10-minute intervals over 24 hours in seven subjects, once with a normal nocturnal sleep from 2300 to 0700 hours, and once with a shifted daytime sleep from 0700 to 1500 hours. The subjects received continuous enteral nutrition and remained supine for the 8 hours preceding blood sampling and throughout the whole experiment. Insulin secretion rate was estimated by deconvoluting peripheral C-peptide levels using an open two-compartment model. The amplitude of glucose and insulin secretion rate oscillations increased by 160% during the 8-hour sleep periods, at whatever time they occurred, whereas the influence of the time of day was not significant. Glucose and insulin secretion rate mean levels were also significantly increased during normal nocturnal sleep compared to the remaining 8-hour waking periods, but this effect did not persist when sleep was shifted to the daytime. The number of oscillations was similar in both experimental series and was not affected by sleep. No systematic concordance was found between glucose and insulin secretion rate oscillations and the rapid eye movement-nonrapid eye movement sleep cycles, despite them having similar periodicities. This study demonstrates that increased amplitude of glucose and insulin secretion rate oscillations is related to sleep rather than to the time of day, without any associated frequency variations.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Renin as a biological marker of the NREM-REM sleep cycle: effect of REM sleep suppression.

We have previously described that, in normal man, the nocturnal oscillations of plasma renin activity (PRA) exactly reflect the rapid eye movement (REM)-non(N)REM sleep cycles, with increasing PRA levels during NREM sleep and decreasing levels during REM sleep. This study was carried out to determine whether REM sleep suppression affects nocturnal renin profiles and to define which sleep stage is essential for renin release. In a first experimental series, REM sleep was suppressed by using clomipramine, a tricyclic antidepressant. Seven healthy young men were studied once during a night when a placebo was given and once during a night following a single dose of 50 mg clomipramine. Blood was collected every 10 min from 23.00 hours to 07.00 hours. PRA was measured by radio-immunoassay and the nocturnal profiles were analysed using the pulse detection program ULTRA. Clomipramine suppressed REM sleep in all subjects but one, but did not affect the number of SWS episodes nor their duration. Similar PRA profiles were observed in both experimental conditions. Neither the mean levels, nor the number and the amplitude of the oscillations were modified and the normal relationship between slow wave sleep and increasing PRA levels was preserved. In a second experimental series, REM sleep was prevented by rapidly awakening the subjects as soon as they fell into REM sleep. The four subjects studied attempted several times to go into REM sleep, but only when PRA levels were decreasing. The interruption of REM sleep by short waking periods did not disturb PRA for which the oscillations remained unaffected. Again, the relationship between SWS and increasing PRA levels was preserved. These results provide evidence that mechanisms increasing slow-wave activity are principally involved in increasing PRA levels and that replacing REM sleep by waking periods and light sleep does not modify nocturnal PRA oscillations.

Journal Article↗
PubMed1994

Twenty-four-hour profiles of plasma renin activity in relation to the sleep-wake cycle.

OBJECTIVE: To evaluate the relative contribution of sleep and the endogenous circadian rhythmicity in producing the 24-h variations in the plasma renin activity. METHODS: Ten normal young men were studied, under basal conditions with normal nocturnal sleep from 2300-0700 h and once after a night of total sleep deprivation followed by 8 h daytime sleep from 0700 to 1500 h. Plasma renin activity was measured every 10 min for 24 h and the profiles were analysed using the pulse detection program ULTRA. RESULTS: During the 8 h night-time sleep a significant increase in the mean plasma renin activity levels occurred compared with the subsequent 8-h waking periods. After the shift in the sleep period, a sleep-associated increase was clearly apparent during the daytime hours. The number of the amplitude of the oscillations, linked to the non-rapid eye movement-rapid eye movement sleep cycles, increased during sleep (at whatever time it occurred), and were dependent on the regularity and the length of the sleep cycles. In awake subjects the plasma renin activity generally fluctuated in a more damped and irregular manner, but occasionally the plasma renin activity oscillated at a regular periodicity with two dominant peaks centred around 100 and 50 min. CONCLUSION: These results demonstrate that the 24-h plasma renin activity variations are not circadian in nature but are related to sleep processes, which create the nycthemeral rhythm by increasing both the frequency and the amplitude of the oscillations.

Adult↗
PubMed1993

Continuous positive airway pressure treatment. Effects on growth hormone, insulin and glucose profiles in obstructive sleep apnea patients.

The principal nocturnal GH peak normally coincides with the first episode of slow wave sleep (SWS). Obstructive sleep apnea (OSA) patients have low nocturnal GH levels which may be explained by their poor quality fragmented sleep but other factors are possibly involved. Obesity is frequently associated with OSA, and obese patients also manifest reduced GH secretion. The mechanisms reducing GH levels in obese subjects are not understood, but hyperinsulinaemia is a suggested factor. In this study nocturnal plasma and secretory GH profiles of OSA patients were examined in relation to the quality and quantity of sleep, together with plasma glucose and insulin levels. Eight OSA patients, (BMI 32.7 +/- 2.3 kg/m2), underwent 2 night studies. For one night no treatment was given and for the other continuous positive airway pressure (CPAP) treatment was administered for the first time. Blood was collected continuously throughout each night and plasma GH, insulin and glucose profiles established in 10 min interval samples. From the plasma data a deconvolution model was used to calculate GH secretion rates. Sleep was recorded during the studies. For the non-treatment night GH levels were low and increased significantly with treatment, p = 0.008 for plasma levels and p = 0.02 for secretion rates. Treatment significantly decreased the cumulative apnea duration and increased the quantity of SWS and Rapid Eye Movement (REM) sleep (p = 0.008), but the mean insulin and glucose profiles did not differ between the two nights. Individual GH plasma and secretion rates, on treatment, showed a tendency to correlate with the amount of SWS (p = 0.09).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Role of cardiac innervation in atrial natriuretic peptide secretion in transplanted heart recipients.

To investigate whether cardiac innervation modulates atrial natriuretic peptide (ANP) secretion, we performed acute volume expansion on eight normal and eight matched (age, weight, and total blood volume) transplanted denervated heart patients (Htx), while monitoring fluid-regulating hormone, systemic blood pressure, and echocardiographic atrial area changes. At rest, plasma ANP and guanosine 3',5'-cyclic monophosphate (cGMP) were lower in control subjects than in Htx (45 +/- 16 vs. 103 +/- 35 pg/l and 0.9 +/- 0.3 vs. 3.5 +/- 1.4 pM, respectively; P < 0.001). Plasma active renin, aldosterone, and catecholamines did not differ significantly in the two populations, whereas arginine vasopressin and cortisol were higher in controls (P < 0.01 and P < 0.005). Although volume expansion (+15%) and atrial stretch were similar in the two groups, plasma ANP and cGMP increased significantly only in the Htx group (103 +/- 35 to 189 +/- 69 pg/l and 3.5 +/- 1.4 to 5.8 +/- 1.4 pM, respectively; P < 0.001). The decrease observed for the other hormones was not significant except for arginine vasopressin and cortisol (P < 0.05 and P < 0.001) in the control group. These results support the hypothesis of an inhibitory role of cardiac innervation in biologically active ANP secretion in humans, at rest and after acute volume expansion.

Adult↗
PubMed1993

Nocturnal pituitary hormone and renin profiles during chronic heat exposure.

To establish the principal endocrine systems involved in the initial adaptation to chronic passive heat exposure, responses of the hydromineral and pituitary systems were compared. Nocturnal plasma profiles of growth hormone, prolactin, thyrotropin, and plasma renin activity were determined during a period of prolonged heat exposure designed to simulate a hot climate. Two groups of six male subjects (G1 and G2) were kept for 11 days in a climatically controlled apartment. The G1 group was exposed to 20 degrees C throughout the study, and the G2 group was exposed to 20 degrees C for 5 days and to 35 degrees C for the following 6 days. Blood was collected continuously during the 1st and 10th nights from 2300 to 0700 h and was sampled in 10-min aliquots for hormone analysis. Heat exposure increased the nocturnal mean core temperature (P < 0.02) and stimulated plasma renin activity (P < 0.01) but had little effect on the pituitary hormones except for a small increase in prolactin (P < 0.05). For the G1 group there was no change in hormone profiles. These results demonstrate that the principal initial endocrine system involved in acclimatization to passive heat exposure is the renin-angiotensin system, reflecting counteractive measures against salt and water losses. In contrast, 5 days of continuous heat exposure does not provoke metabolic changes, indicated by the small effect on pituitary hormone profiles.

Adaptation, Physiological↗
PubMed1992

Nocturnal prolactin pulses in relation to luteinizing hormone and thyrotropin.

The two hypothalamic releasing factors, luteinizing hormone releasing hormone (LHRH) and thyrotropin releasing hormone (TRH), have been shown to stimulate pituitary prolactin (PRL) release as well as their respective pituitary hormones, luteinizing hormone (LH) and thyrotropin (TSH). In this study the influence of LH and TSH regulatory mechanisms on nocturnal PRL secretion was investigated by evaluating whether the coincidence of PRL with LH and TSH pulses occurred more frequently than would be expected if the hormone generators were not coupled. Thirty night studies were conducted in twelve healthy male subjects. Six subjects underwent 3 studies and 6 subjects 2 studies. Blood was collected into aliquots at 10 min intervals throughout the night and plasma concentrations of PRL, TSH, and LH were determined. From the plasma profiles, hormone secretory rates were calculated using a method of deconvolution. Significant plasma and secretory hormone pulses were identified by a peak detection computer program. For statistical analysis the night studies of each subject were concatenated. Concomitance between the plasma pulses of both TSH and LH with PRL was insufficient to reject the null hypothesis of random coincidence. An increase in the number of subjects demonstrating significant coincidence between the hormone pulses was obtained when secretory pulses were analysed. Seven of the 12 and 10 of the 12 subjects showed significant concomitance between PRL and respectively TSH and LH. This proportion was sufficient to confirm copulsatility between PRL and LH. These results suggest that LH regulatory mechanisms are involved in the generation of the nocturnal pulsatile PRL profile, TRH may also play a role in the secretion of PRL at a central level, but was not reflected in the plasma or secretory profiles because of other overriding regulatory factors.

Adult↗
PubMed1992

Effect of awakening on aldosterone.

Overnight studies conducted in 10 male volunteers showed that the effect of awakening on aldosterone and its main regulatory hormonal systems depends on the time of its occurrence. Waking periods in the latter half of the night induced concomitant increases in plasma levels of aldosterone and ACTH, whereas plasma renin activity tended to decrease. No effect was apparent, when subjects were awoken during the first hours of sleep, which is known to be a quiescent period of adrenocorticotropic activity. These results provide evidence of the dominant influence of ACTH during the second half of the night insuring the regulation of aldosterone during waking periods.

Adrenocorticotropic Hormone↗
PubMed1992

Lack of diurnal rhythm in plasma atrial natriuretic peptide.

The occurrence of a circadian rhythm in the concentration of circulating atrial natriuretic peptide (ANP) is not clearly established. To investigate diurnal changes, plasma levels of ANP were measured at 10-min intervals for 24 hours in six normal volunteers. The subjects were studied once during a normal sleep-wake cycle and once during a cycle with a shifted sleep period. They received continuous enteral nutrition from 8 hours preceding the experiment until the end of the experiment, throughout this time the subjects remained in a supine position. The mean ANP levels did not differ significantly between the sleep periods and the periods spent awake in either of the protocols, which provides evidence of a lack of a sleep-related influence of ANP. A significant linearity of the mean ANP profile was observed, smoothing out the transient and randomly occurring fluctuations in individual ANP concentration. These results lead to the conclusion that ANP secretion is neither under the control of endogenous circadian rhythmicity nor is it affected by sleep-regulatory mechanisms.

Adult↗
PubMed1992

Nocturnal cortisol release in relation to sleep structure.

The relationship between the temporal organization of cortisol secretion and sleep structure is controversial. To determine whether the cortisol profile is modified by 4 hours of sleep deprivation, which shifts slow-wave sleep (SWS) episodes, 12 normal men were studied during a reference night, a sleep deprivation night and a recovery night. Plasma cortisol was measured in 10-minute blood samples. Analysis of the nocturnal cortisol profiles and the concomitant patterns of sleep stage distribution indicates that the cortisol profile is not influenced by sleep deprivation. Neither the starting time of the cortisol increase nor the mean number and amplitude of pulses was significantly different between the three nights. SWS episodes were significantly associated with declining plasma cortisol levels (p less than 0.01). This was especially revealed after sleep deprivation, as SWS episodes were particularly present during the second half of the night, a period of enhanced cortisol secretion. In 73% of cases, rapid eye movement sleep phases started when cortisol was reflecting diminished adrenocortical activity. Cortisol increases were not concomitant with a specific sleep stage but generally accompanied prolonged waking periods. These findings tend to imply that cortisol-releasing mechanisms may be involved in the regulation of sleep.

Adult↗
PubMed1992

Plasma renin activity and sleep-wake structure of narcoleptic patients and control subjects under continuous bedrest.

In order to determine if renin release would be affected by a dysfunction of the circadian and ultradian organization of sleep, 24-hour profiles of plasma renin activity (PRA) concomitant with sleep stages were established in 10 normal subjects and nine narcoleptic patients, with 10-minute blood sampling intervals. Mean PRA levels were similar in control subjects and narcoleptic patients. Individual 24-hour profiles revealed that the previously described association between renin oscillations and sleep stage alternations was preserved. Increased PRA release was observed during the transition from rapid eye movement (REM) sleep or waking periods to nonrapid eye movement (NREM) sleep, and REM sleep occurred as PRA levels were decreasing. Thus, PRA curves exactly reflected the irregularities and disturbances in the sleep structure of the narcoleptic patients. The 24-hour PRA profiles of the patients did not show the general upward trend during nighttime sleep, which is probably induced in the control subjects by the repetitive recurrence of longer episodes of undisturbed NREM sleep. Because of marked sleep fragmentation in the patients, the duration of NREM sleep was often insufficient to allow for the occurrence of a significant PRA increase. Because sleep onset REM (SOREM) episodes, characteristic of narcolepsy, are not preceded by NREM sleep and its associated increase in PRA, no relative PRA decline occurred during this type of REM sleep. In conclusion, the 24-hour PRA profiles of the narcoleptic patients reflected exactly their sleep stage distribution, confirming previous findings that PRA oscillations appear to be inseparable from the NREM-REM sleep cycle.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Nocturnal plasma thyrotropin variations are related to slow-wave sleep.

The thyrotropin (TSH) nycthemeral pattern is known to be strongly influenced by sleep, but previous studies have failed to demonstrate any link between sleep structure and TSH variations. Using 10-min blood sampling, nocturnal TSH profiles were analysed in 24 young healthy subjects during normal sleep. Six of the subjects then underwent a partial sleep deprivation experiment, sleep was permitted from 03.00 hours to 07.00 hours. Descending slopes of TSH values were observed for the first 20 minutes of SWS episodes, whereas no significant trend was found for other sleep stages. During the period of sleep deprivation, nocturnal TSH levels increased and then declined immediately after sleep onset; however, the association between SWS and descending TSH slopes persisted. This temporal concordance suggests that some particular mechanisms associated with SWS may modulate TSH release, or conversely that increasing TSH levels prevent the occurrence of SWS.

Journal Article↗
PubMed1991

Alteration in the temporal organisation of insulin secretion in type 2 (non-insulin-dependent) diabetic patients under continuous enteral nutrition.

Concomitant oscillations of plasma glucose, insulin and C-peptide levels with a period of about 80 min between peak levels have been identified in normal man. To determine whether these oscillations persist in Type 2 (non-insulin-dependent) diabetic patients, peripheral plasma levels of glucose, insulin and C-peptide were measured at 10 min intervals over 12 h in six patients and in six matched control subjects during continuous enteral nutrition (90 kcal.h-1;50% carbohydrate, 35% fat, 15% protein). The insulin secretion rate was estimated from peripheral C-peptide levels using an open two-compartment model. For the control subjects, mean plasma glucose, insulin and insulin secretion profiles rose sharply and then attained a steady-state; in contrast, for the diabetic patients, the mean insulin and insulin secretion profiles were characterized by a slow ascending trend throughout the day. Mean glucose levels rose sharply and reached higher levels than in the control subjects. The individual 12 h profiles revealed synchronous oscillations of plasma glucose, plasma insulin, and insulin secretion in the control subjects. In the diabetic patients, the number of plasma insulin and insulin secretion pulses was significantly lower; they had a smaller amplitude and were less frequently associated with the glucose pulses. However, plasma glucose levels had a similar oscillatory pattern in the diabetic patients compared with the control subjects, albeit with a higher absolute amplitude. The poor association between glucose and insulin secretion pulses in the diabetic patients suggests that insulin pulses are insufficient to account for the glucose pulses.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Effects of treatment with nasal continuous positive airway pressure on atrial natriuretic peptide and arginine vasopressin release during sleep in patients with obstructive sleep apnoea.

1. Patients with obstructive sleep apnoea have increased diuresis during sleep, which decreases with nasal continuous positive airway pressure treatment. These changes have been attributed to an increased release of atrial natriuretic peptide in obstructive sleep apnoea, and its decrease with continuous positive airway pressure treatment. 2. In order to clarify the change in plasma atrial natriuretic peptide level and to investigate the underlying mechanisms, blood samples were taken at 10 min intervals from nine patients with obstructive sleep apnoea during two nights when the patients were either untreated or treated with continuous positive airway pressure. Polysomnographic monitoring, including transcutaneous oximetry, and measurement of oesophageal pressure were performed simultaneously. Plasma arginine vasopressin was also measured. 3. The plasma level of arginine vasopressin did not change. The level of atrial natriuretic peptide was high and exhibited secretion bursts in six out of the nine patients; it drastically decreased with continuous positive airway pressure treatment. 4. Across the patients, the mean plasma levels of atrial natriuretic peptide was correlated with the degree of hypoxaemia and the degree of oesophageal pressure swings during the sleep apnoeas. 5. Within the patients, cross-correlation studies suggested that the atrial natriuretic peptide secretory bursts were related either to the oesophageal pressure swings or to the apnoea-related hypoxaemia. 6. We conclude that release of atrial natriuretic peptide decreases with continuous positive airway pressure treatment in those patients with obstructive sleep apnoea who have increased release of atrial natriuretic peptide before treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Obstructive sleep apnea treatment: peripheral and central effects on plasma renin activity and aldosterone.

To assess the effect of obstructive sleep apnea treatment on plasma renin activity (PRA) and plasma aldosterone seven male patients were studied under two conditions: untreated and treated with nasal continuous positive airways pressure (CPAP). PRA and plasma aldosterone were measured at 10-min intervals for both nights. CPAP treatment diminished the urinary and Na+ excretion, whereas plasma volume increased. The mean levels of PRA and aldosterone were significantly enhanced by the treatment, increasing respectively from 1.5 +/- 0.3 to 3.0 +/- 0.7 ngAI ml-1.hr-1 (p less than 0.05) and from 8.0 +/- 1.0 to 12.0 +/- 1.7 ng.100 ml-1 (p less than 0.05). PRA curves reflected the overall sleep structure as similarly described in normal subjects. The apnea-induced sleep disturbance led to flat PRA profiles and the restoration of a normal sleep pattern by treatment restored the PRA oscillations related to the sleep cycles and consequently restored aldosterone oscillations. The mean amplitude of these oscillations increased respectively from 1.0 +/- 0.1 to 1.8 +/- 0.4 ngAI ml-1.hr-1 and from 5.4 +/- 1.2 to 10.9 +/- 1.9 ng.100 ml-1. These results suggest that CPAP treatment modifies the nocturnal patterns of PRA and aldosterone by increasing their mean levels and their oscillation amplitude. This indicates increased secretion, which contributes to the normalization of urine and Na output.

Adult↗