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Biomedical subjects

D Riemann

Publications and source records attributed to D Riemann.

At least 163 records · Page 9Linked to original sources
PubMed1989

EEG sleep in depression and in remission and the REM sleep response to the cholinergic agonist RS 86.

A comparison of the sleep EEG patterns of patients with a major depressive disorder intraindividually between remitted and depressed state revealed an improvement of parameters of sleep continuity and a tendency for normalization of rapid eye movement (REM) latency and REM density in the former. Additional application of the cholinergic agonist RS 86 prior to sleep did not reveal a heightened sensitivity of the REM sleep system in the remitted sample. Whereas a group of presently ill depressives displayed a drastic reduction of REM latency, results of the remitted patients were comparable to healthy controls. Furthermore, RS 86 significantly reduced slow-wave sleep in all groups investigated and had a differential impact on the density of the first REM period and early morning awakening in actively ill patients as compared to remitted patients. The results do not favor the hypothesis of a trait specificity of REM sleep abnormalities for depressive disorders. Furthermore they support the model of a cholinergic supersensitivity, as measured by REM induction after RS 86, as a state but not a trait marker of affective illness. Generalization of the present study may, however, be limited by the fact that the remitted patients were free of symptomatology and psychoactive medication for a long period (mean 3 years), therefore constituting an untypical group of formerly depressed patients with a seemingly low risk of relapse.

Adult↗
PubMed1989

[Sleep in anorexia nervosa, bulimia nervosa and depressive diseases: a polysomnographic comparative study].

All-night EEG sleep in 20 anorexics, 10 bulimics, 10 endogenous depressives, and in 10 healthy subjects (all age matched) was compared. In addition, the REM sleep-induction-test was performed in 12 patients with an eating disorder, 7 depressives, and 12 controls by application of the cholinergic agent RS 86. During baseline night, EEG-sleep parameters, especially REM latency, did not differ between the patients and the controls, except for the phasic components of REM sleep (REM density) that were increased in the depressive patients. The frequency of shortened REM latencies, however, was significantly higher in the depressed patients. These observations indicate that in some of the young depressives the disturbance of the REM sleep regulating transmitter system is already present to a similar degree as it is assumed in elderly depressives. After the application of RS 86, REM latency was shortened in all groups under investigation. However, the REM sleep inducing effect of RS 86 was significantly more pronounced in the depressives when compared with both the eating disorder patients and the controls. In the latter two samples, the shortening of REM latency was similar. Furthermore, the eating disorder patients with a concomitant major depression reacted similar to RS 86 as the non-depressed eating disorder patients and the control subjects. Whereas baseline EEG-sleep did not differ significantly among eating disorder patients, young depressives, and healthy subjects, the REM sleep inducing effect of the cholinergic agent RS 86 clearly distinguished between the depressives and both the patients suffering from eating disorders and the controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Effects of fasting and glutathione depletors on the GSH-dependent enzyme system in the gastrointestinal mucosa of the rat.

In rats, the glutathione content of the gastrointestinal mucosa amounted to 50-60% of that of the liver. The GSH-S-transferase activity towards an aryl substrate (CDNB) was low in the stomach, colon and rectum, i.e. 5% of hepatic activity. In the small intestine there was a typical decline of activity from proximal to distal segments. GSH-Peroxidase was much lower in the intestinal mucosa as compared to the stomach and liver, whereas the GSSG-reductase was 2-3 times higher in the gastrointestinal tract in comparison to the liver. Fasting for 24 h significantly decreased the GSH content, GSH-aryltransferase and GSSG-reductase activities in the liver but not in the intestine, where even higher GSH concentrations were found in the proximal segments. L-Buthionine-sulfoximine, an inhibitor of the GSH-synthesis, caused a marked decrease of the GSH levels in the liver, stomach, proximal small intestine, colon and rectum and a concomitant decline in GSSG-reductase activity. Among the GSH-depleting agents, paracetamol exerted the strongest effect, whereas 1,1-dichloroethylene and phorone only decreased the GSH content in the liver and stomach.

Animals↗
PubMed1989

A simple but highly sensitive radioreceptor assay for the determination of scopolamine and biperiden in human plasma.

Simple and sensitive methods are described for the determination of scopolamine and biperiden in human plasma. Each method consists of two steps. After extraction of scopolamine and biperiden with chloroform or n-hexane respectively and evaporation of the organic solvent, both drugs are determined by their ability to inhibit the specific binding of tritiated N-methyl-scopolamine to mouse brain homogenates. The lower limits of detection are plasma levels of about 50 pg/ml scopolamine and about 200 pg/ml biperiden.

Animals↗
PubMed1988

Influence of the cholinergic agonist RS 86 on normal sleep: sex and age effects.

In 36 healthy control subjects (21 females, 15 males; age range 18-65 years; mean age 41.8 years, SD 15.6 years), a bedtime dose of 1.5 mg RS 86, an orally acting cholinergic agonist, shortened rapid eye movement (REM) latency, increased REM sleep, and decreased slow-wave sleep. Six of the subjects (greater than 40 years old) even displayed sleep-onset REM periods after the drug. Results of the present study agree well with those of studies using other cholinomimetics (i.e., physostigmine, arecholine) and confirm the importance of the cholinergic system for REM sleep regulation. Since RS 86 mimicked some of the REM sleep abnormalities specific for patients with depressive disorders, the cholinergic system may play a role in the pathogenesis and pathophysiology of depressive diseases.

Adolescent↗
PubMed1988

EEG sleep and the cholinergic REM induction test in anorexic and bulimic patients.

The electroencephalographic (EEG) sleep of 20 anorexic patients, 10 bulimic patients, and 10 age-matched healthy controls was studied. In addition, six anorexic patients and six bulimic patients had a cholinergic rapid eye movement (REM) sleep induction test (RIT) performed with the cholinergic agent RS 86. The three samples showed no major differences in sleep patterns. The same held true when attention was focused on patients who additionally met DSM-III criteria for major depression. The RIT results were similar in the patients with eating disorders and in controls, but differed from those reported in depressives. Therefore, the present study found no hints of depression-like sleep patterns in patients with eating disorders.

Adult↗
PubMed1988

Glutathione and GSH-dependent enzymes in the gastrointestinal mucosa of the rat.

The mucosal glutathione content of the gastrointestinal wall amounted to 50-60% of its concentration in the liver. GSH S-aryltransferase activity (CDNB) was very low in the glandular stomach, colon and rectum amounting to only 5% of liver enzyme activity. There was a marked postpyloric increase in GSH S-aryltransferase activity with an oral-aboral decline along the small intestine. GSH peroxidase was much lower in the mucosa of the small and large intestine as compared to the stomach or liver, whereas GSSG reductase was more than twice as high in the gastrointestinal mucosa as compared to the liver showing a gradual increase in activity from proximal to distal segments. The low GSH S-transferase activities found in the stomach, colon and rectum may account for the high and exclusive susceptibility of these segments to carcinogenesis and the deficient inducibility of these enzymes in the gastrointestinal wall may reflect an insufficient adaption towards higher exposure to toxic or even carcinogenic xenobiotics.

Animals↗
PubMed1987

Serotonin reuptake inhibition vs. norepinephrine reuptake inhibition: a double-blind differential-therapeutic study with fluvoxamine and oxaprotiline in endogenous and neurotic depressives.

The antidepressive properties of the specific serotonin reuptake inhibitor fluvoxamine and the specific norepinephrine reuptake inhibitor oxaprotiline were investigated in a sequential design with the aim of evaluating the hypothesis that two distinct biochemical subtypes of depression exist. Responders were treated for 7 weeks with the compound to which they had responded. After 1 placebo week, the nonresponders were switched to the alternative compound. An evaluation of the data obtained during the 3-week treatment periods from 24 patients (37 trials) with major depression revealed a highly significant reduction of Hamilton Scores with both compounds, oxaprotiline and fluvoxamine. If the patients with major depression are subdivided into two groups, endogenous depressives and neurotic depressives, there is no significant difference between the therapeutic improvements (both compounds) achieved in the two groups. The data shows that only about 20% of the nonresponders on one compound responded to the alternative drug, whereas 90% of responders (within 3 weeks) were still responders after 7 weeks. The data are at variance with the concept of two distinct biochemical subtypes of depression (serotonergic vs. norepinephrinergic). Dexamethasone suppression tests, performed in 23 patients, gave no prognostic hint as to whether the patients reacted well to drug therapy or not.

Adult↗
PubMed1987

Sleep and dreams in eating disorders.

The results of several studies on sleep EEG and dreams in patients with eating disorders are presented and compared with the data obtained in patients with a major depression. The sleep pattern, which is characteristic of depression, could not be found in the eating disorder group. Regarding the cholinergic REM induction test, the depressive displayed a pronounced shortening of REM sleep latency. However, this biological marker, indicating a cholinergic hyperactivity in depression, could not be observed in patients with eating disorders. The content analysis of laboratory-recorded dreams yielded several differences between depression and eating disorders and also, more subtle, between anorexia and bulimia.

Anorexia Nervosa↗
PubMed1986

Is there a relationship between response to total sleep deprivation and efficacy of clomipramine treatment in depressed patients?

Total sleep deprivation (TSD) and tricyclic medication are successful treatment modalities for patients with a major depressive disorder. Recent studies have suggested a positive relationship between TSD response and succeeding tricyclic treatment, even on a very specific level, thus supporting the assumption of two distinct biochemical subtypes of depression. The present study tested this hypothesis by treating 10 inpatients with a major depressive disorder first with TSD and succeedingly with clomipramine. Contrary to expectation, a negative relationship between clinical response to the two treatment modalities was found.

Adolescent↗
PubMed1986

The nature of neuroendocrine abnormalities in depression: a controversial issue in contemporary psychiatry.

Neuroendocrine abnormalities in depression have been regarded, by many authors, as relatively specific markers of nosological subtypes of the disorder, e.g. primary vs. secondary, endogenous vs. non-endogenous or unipolar vs. bipolar depression. They should reflect the same changes in central neurotransmitters (e.g. noradrenergic insufficiency and/or cholinergic hyperactivity) that were hypothesized as the cause of clinical symptoms. This view is challenged on the basis of our own neuroendocrine investigations in 317 psychiatric patients and 103 normal controls. According to these studies the abnormalities are nosologically rather unspecific. They are induced by a large variety of factors, e.g. emotional stress associated with the clinical symptomatology, weight loss due to malnutrition as a consequence of reduced appetite, medication and drug withdrawal. Stress-induced hypercortisolism appears to be the most common abnormality that may trigger other neuroendocrine dysfunctions, such as a blunted TSH response to TRH. Differences in neuroendocrine abnormalities of depressives are probably due to variations in the manifold factors influencing the hormonal axes involved, to temporal changes in hormonal patterns (e.g. one abnormality triggering another) and to individual differences in the basic activity and the responsiveness of the various axes.

Adrenocortical Hyperfunction↗
PubMed1981

Surface hydrophobicity of proteins and selectivity of intracellular proteolysis.

The affinity of cytosol proteins from protein-free fed rats to hydrophobic surfaces is diminished in comparison to the affinity of cytosol proteins from normal or protein-rich fed rats. Furthermore, the affinity of these cytosol proteins to hydrophobic surfaces in the presence of ultrafiltrates from cytosol of rats fed previously a protein-rich diet or a protein-free diet is diminished. Ultrafiltration itself increases the affinity of cytosol proteins to hydrophobic surfaces (octyl-sepharose or phenyl-sepharose).

Animals↗