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Biomedical subjects

K Adam

Publications and source records attributed to K Adam.

At least 55 records · Page 3Linked to original sources
PubMed1986

The hypnotic effects of an antihistamine: promethazine.

Twelve volunteer poor sleepers of mean age 59 years took placebo on one night, promethazine 20 mg on one night and promethazine 40 mg on one night, in a double-blind balanced order study. Sleep in the EEG laboratory was increased by nearly 1 h after either dose of promethazine, and sleep interruptions were reduced. Slow-wave sleep was unaffected, but the larger dose reduced the percentage of sleep spent as REM sleep. Sleep was improved subjectively by both doses of promethazine which appears to be an effective hypnotic.

Aged↗
PubMed1986

Effects of paroxetine on human sleep.

In a first double-blind, balanced order study, 12 subjects, mean age 57 years, took placebos at bedtime on 2 nights, paroxetine 15 mg on 2 nights and paroxetine 30 mg on 2 nights. In a second study, 12 subjects, mean age 56 years, took placebos on 2 mornings and paroxetine 30 mg on 2 mornings. Electrophysiological measures of all-night sleep were made on each night subsequent to medication. Paroxetine caused more frequent awakenings, reduced total sleep and strongly suppressed REM sleep, especially the 30 mg dosage. When it had been taken in the morning, paroxetine additionally delayed sleep onset and increased slow-wave sleep.

Adult↗
PubMed1984

Are poor sleepers changed into good sleepers by hypnotic drugs?

Sleep can be measured by subjective ratings, electrophysiological recordings and by the physiological and biochemical changes occurring with sleep. Using these methods, we can select those who rate their sleep as unsatisfactory and those who feel fully satisfied by their sleep. Electrophysiological recordings of sleep show that there are relatively small differences between these good and poor sleepers: poor sleepers sleep less than good sleepers, but not as little as they think. However, the complaints of poor sleepers that they feel unrestored by their sleep should not be dismissed, for investigations employing the tools of physiology and biochemistry have revealed differences between good and poor sleepers that suggest that the sleep of poor sleepers may indeed be less restorative. The actions of hypnotic drugs on sleep can be similarly investigated. Preliminary findings suggest that hypnotic drugs may reverse some of the detrimental metabolic concomitants of poor sleep.

Biological Clocks↗
PubMed1984

Effect of loprazolam and of triazolam on psychological functions.

Twelve poor sleepers of mean age 52 years performed 2 h of laboratory tests three times on 1 day during each week of nightly intake of loprazolam 0.5 mg, loprazolam 1 mg, triazolam 0.5 mg, or continued placebos. Only in the mornings did loprazolam 1 mg cause impairment in manual dexterity and card-sorting, and triazolam 0.5 mg in manual dexterity. Using difference from baseline, withdrawal of either drug after 3 weeks was associated with poorer subjective quality of sleep than following continuing placebos. The rate of spontaneous complaints (including accidents) associated with the drugs was as informative as formal testing.

Adult↗
PubMed1984

Effects of loprazolam and of triazolam on sleep and overnight urinary cortisol.

Nine poor sleepers of mean age 61 years were studied while they took loprazolam 0.5 mg, loprazolam 1 mg and triazolam 0.5 mg for 3-week periods. Loprazolam 1 mg and triazolam 0.5 mg increased sleep duration, but there was some tolerance to both, particularly triazolam, by the 3rd week. Withdrawal of either drug led to sleep significantly shorter than baseline. This rebound effect was significant greater than withdrawing triazolam. After withdrawing loprazolam 1 mg, the rebound was maximal on the 3rd night and after withdrawing triazolam it was maximal and severe on the 1st night. In the third week of use neither drug was associated with late-night wakefulness. Total overnight urinary cortisol was lower during drug intake and there were significant withdrawal rebounds to above baseline levels, immediately so after triazolam.

Aged↗
PubMed1984

[Endogenous nitrogen metabolism in 15N-labeled swine. 1. Course of 15N-labeling and 15N excretion in urine and feces under 4 different diets].

Four male castrated pigs (55-65 kg) either received a wheat--fish meal diet (1 and 2) or a wheat--horse bean diet (3 and 4) without straw meal supplement (1 and 3) or with a supplement of 20% DM partly hydrolysed straw meal to the DM of the ration (2 and 4). In order to investigate whether a 15N-labelling of the pigs is also possible with a protein excess in the ration, the animals 1 and 2 received 24.8 g and the animals 3 and 4 = 11.6 g crude protein/kg0,75 live weight. During a 10-day 15N-labelling 385 mg 15N-excess (15N') per kg0,75 were applied in a mixture of ammonia acetate and ammonia chloride in the feed. During the period of 15N-labelling the following quotas of the applied 15N-amount were incorporated: 1 = 10.2%, 2 = 7.2%, 3 = 18.7%, 4 = 14.4%. 15N-excretion in both TCA fractions of faeces showed a highly significant positive correlation to the increasing content of crude fibre in the 4 diets. The immediate 15N-incorporation into the TCA-precipitable fraction of faeces (from the 2nd of the beginning of the 15N-application onwards) proves that 15N enters the large intestine endogenously (probably as 15N-urea) and serves bacterial protein synthesis. Three days after the last 15N-application the pigs were killed. The following values of atom-% 15N' could be determined in the TCA-precipitable blood plasma and in the TCA-precipitable fraction of the liver: 1 = 0.18 and 0.19 resp., 2 = 0.22 and 0.27 resp., 3 = 0.22 and 0.23 resp. and 4 = 0.24 and 0.26 resp. The other examined organs and tissues showed smaller differences between the test animals. The following atom-% 15N' were measured in the TCA-precipitable fractions on an average of the 4 test pigs: kidney = 0.20, pancreas = 0.18, intestinal wall tissue, duodenum = 0.18, jejunum (beginning) = 0.17, jejunum (end) = 0.15, ileum = 0.15, caecum = 0.16, colon (beginning) = 0.15, colon (middle) = 0.14, colon (end) = 0.13, stomach (cardia) = 0.11, stomach (fundus) = 0.12, spleen = 0.13, heart = 0.12, skin = 0.07 and skeleton muscles = 0.06. The results show that the 15N-labelling of tissues and organs of pigs is also possible at a high level of protein supply by means of an oral application of 15N ammonia salts.

Animals↗
PubMed1984

Effect of physical fitness and body composition on sleep and sleep-related hormone concentrations.

The study assessed the effect of physical fitness and body composition on sleep and the nighttime secretion of the hormones, human growth hormone (hGH), prolactin, and cortisol. Two groups of 17 subjects, one of fit athletes and the other of unfit nonathletes, were selected so that the groups were matched for weight, height, lean body mass (LBM), and fat levels. Subjects slept in a sleep laboratory for 3 nonconsecutive nights: 1 adaptation night and 2 experimental nights. On 1 experimental night blood samples were collected; on the other, baseline sleep was assessed and the catheter was not inserted. Weight and height were measured and LBM assessed by 24 h urinary creatinine. The effect of physical fitness was tested by a comparison of the two groups; body composition was assessed by correlation analyses. Physical fitness did not have a significant effect on either sleep or hormone levels, although in the latter case the results were marginal. In contrast, body composition was related to both sleep and hGH. Percentage LBM was negatively correlated with slow-wave sleep and positively correlated with hGH levels. These results were significant for all subjects combined and for the fit group, although not the unfit group alone.

Adipose Tissue↗
PubMed1984

Effects of lormetazepam and of flurazepam on sleep.

Nine poor sleepers of mean age 61 years took part in a double-blind, balanced order study in which, during three periods of 3 weeks, each took lormetazepam 1 mg, lormetazepam 2.5 mg, and flurazepam 30 mg. Using electrophysiological measures, sleep was found to increase by 0.75 h with each treatment condition, mainly through more of stage 2 sleep. The treatments reduced the delay to sleep and led to fewer and shorter awakenings, with little difference among the three treatments. Slow-wave sleep was reduced by flurazepam and by lormetazepam 2.5 mg. After flurazepam intake ceased, there was evidence of persisting drug effects for as long as 7 nights. In contrast, when lormetazepam 2.5 mg ceased, there was significant rebound reduction of sleep duration below baseline for up to 3 withdrawal nights, and there was a similar though non-significant trend after lormetazepam 1 mg had ceased. Wakefulness in the final 2 h of nocturnal recording during the third week of drug intake was significantly reduced below baseline by flurazepam, but was little affected by lormetazepam. The differences among the treatment conditions could be attributed to the long-persistence of flurazepam vs the more rapid elimination of lormetazepam.

Aged↗
PubMed1983

Trazodone enhances sleep in subjective quality but not in objective duration.

Nine volunteer poor sleepers, of mean age 61 years, took trazodone 150 mg nightly for 3 weeks, preceded by 2 weeks and followed by 1 week of matching blanks, in order to examine the effects of electrophysiologically-recorded and subjectively-rated sleep. The second of the initial weeks of matching blanks served as a baseline week. In the subjective ratings, sleep improved in quality on trazodone, significantly so in the first and second weeks of intake, though with significant rebound insomnia on the second withdrawal night. Trazodone halved the frequency of arousals interrupting sleep, and it reduced the time spent in stage 1 (drowsiness). It increased the duration of slow-wave sleep (stages 3 + 4), with a negative rebound following withdrawal. It reduced the time spent in REM sleep, with a rebound above baseline levels after withdrawal. Trazodone did not change total sleep duration, nor the time required to fall asleep. The effects of trazodone were sustained or became enhanced during the period of intake. They persisted for over 24 h after the last dose, and rebound effects were maximal on the second withdrawal night.

Aged↗
PubMed1983

[Scanning electron microscopy studies of the structure of calcium oxalate urinary calculi].

The examination of calcium oxalate calculi under a scanning electron microscope confirmed the 4 structural types distinguished under a polarising microscope using microsections. The fine structure of the radial-concentric-shelled structural type I is characterized as a dense pack of radially ordered prismatic bundles. In combination with energy-dispersive analysis the occurrence of the finely crystalline type II is confirmed. Energy-dispersive analysis shows an unexpected variety of element distribution in the microscopic range.

Calcium Oxalate↗
PubMed1982

Benzodiazepine hypnotics remain effective for 24 weeks.

Ninety-seven poor sleepers aged 40-68 years took capsules nightly for 32 weeks and made daily subjective ratings. The benzodiazepine hypnotics lormetazepam 2 mg and nitrazepam 5 mg appeared still to improve sleep after 24 weeks of intake when compared with continuous placebo intake. The sustained effectiveness was most evident in a significant shortening of the time taken to fall asleep in patients receiving lormetazepam. After weeks, sleep latency and the quality of sleep were significantly worse than baseline values. The impairment was maximal on the second night after withdrawal of lormetazepam and on the fourth night after withdrawal of nitrazepam. It is concluded that benzodiazepines remain effective for at least 24 weeks but that a period of disturbed sleep may be expected after withdrawal.

Adult↗
PubMed1982

Human EEG slow-wave sleep increased by a serotonin antagonist.

Serotonin has been held to play a necessary role in EEG slow-wave sleep. A central serotonin antagonist, known as FU 29-245, 200 mg, was taken nightly for 6 nights by 10 volunteers, mean age 59 years. Compared with baseline sleep the drug significantly increased the duration of slow-wave sleep, with a significant rebound decrease below baseline after withdrawal. The drug also caused fewer transitions into stage 1 and less time in stage 1 and less time in stage 2. There were significant tolerance effects by the fifth and sixth nights. No subjective effects were present.

Adult↗