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Biomedical subjects

P Plenge

Publications and source records attributed to P Plenge.

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

Chlorimipramine--but not imipramine--rapidly reduces [3H]imipramine binding in human platelet membranes.

A single dose of 50 mg chlorimipramine was followed by a rapid and pronounced decrease in [3H]imipramine binding to platelet membranes. Incubation of human platelets or platelet membranes with 25 nM chlorimipramine similarly reduced [3H]imipramine binding. Imipramine, desmethylchlorimipramine, chlorpromazine and some serotonin uptake inhibitors did not have this effect. The effect was not due to chlorimipramine remaining in the membranes during the binding analysis.

Amitriptyline↗
PubMed1986

High affinity binding of 3H-paroxetine and 3H-imipramine to rat neuronal membranes.

Paroxetine is the most potent and one of the most specific serotonin uptake inhibitors. High-affinity 3H-paroxetine and 3H-imipramine binding was compared in rat neuronal membranes. The KD value for 3H-paroxetine binding to neuronal membranes was 0.08 nM, which is exactly the same value as with platelet membranes. The KD value for 3H-imipramine binding to neuronal membranes was about 4 nM, which is higher than the KD value for 3H-imipramine binding to platelet membranes (0.5 nM). The results indicated that the 3H-paroxetine binding site is identical in neuronal membranes and in platelet membranes; this binding site is probably located on the serotonin transport mechanism. In addition, part of the high-affinity 3H-imipramine binding to neuronal membranes is probably located on the serotonin transport mechanism, but another part is located elsewhere. Furthermore the polypeptides containing the 3H-imipramine binding sites may not be identical in neuronal and platelet membranes.

Animals↗
PubMed1985

Antidepressive drugs can change the affinity of [3H]imipramine and [3H]paroxetine binding to platelet and neuronal membranes.

Serotonin transport in synapses and platelets is inhibited by tricyclic antidepressants as well as by more selective transport inhibitors. This inhibition is hypothesized to be of importance for the psychotropic effect, although it is known that some new antidepressants do not possess this transport inhibitory action. We now report that antidepressive drugs can influence the serotonin transport complex in platelets and brain in other ways: [3H]imipramine and [3H]paroxetine, which bind with high affinity to the serotonin transport complex, can be dissociated from the complex with velocity constants strongly influenced by the different antidepressants. This effect is not correlated to the inhibitory action of the drugs on serotonin transport. Furthermore the effect is seen in the micromolar range in contrast to the high affinity binding process which takes place in the pico- and nanomolar range. The effects of antidepressants on the dissociation rates of bound ligand make it possible to differentiate between serotonin reuptake inhibitors which appear identical in other assays. Antidepressive drugs can thus be divided into groups which differ from the usual classifications.

Animals↗
PubMed1985

Serum lithium minimum and diuresis.

Serum lithium was analyzed over a 24-hour period in patients who were receiving lithium in one daily dose. Linear regression was performed with urine volume as the independent variable and lithium dose, maximum serum lithium concentration. 12-hour serum lithium, minimum serum lithium, length of treatment, and age of patients as the dependent variables. Only minimum serum lithium and urine volume showed a good positive correlation.

Adult↗
PubMed1984

Size determination of binding polymers for [3H]imipramine and [3H]paroxetine in human platelet membranes.

Imipramine and paroxetine both inhibit the transport of serotonin in serotonergic neurons and in platelets; furthermore specific high affinity binding sites for [3H]imipramine and [3H]paroxetine are located in these two cell types, probably on the serotonin transport mechanism. However, previous studies indicated that the binding site for [3H]imipramine was different from the binding site for [3H]paroxetine. We now report that the polymers on which the two binding sites are located have different molecular weights.

Blood Platelets↗
PubMed1984

Imipramine binding site. Temperature dependence of the binding of 3H-labeled imipramine and 3H-labeled paroxetine to human platelet membrane.

The characteristics of 3H-labeled imipramine and 3H-labeled paroxetine binding to human platelet membranes were determined at various temperatures between 0 and 37 degrees C. Both paroxetine and imipramine probably bind to the same molecular complex in the platelet membrane, but the binding characteristics are different for the two molecules. The dissociation constant (Kd) for imipramine increases from 0.3 nM to 7.0 nM with increasing incubation temperature in a continuous way, whereas Kd for paroxetine is almost constant, about 0.05 nM, between 0 and 19 degrees C, and first begins to increase from 0.06 nM to 0.16 nM between 20 and 37 degrees C. This suggests that the binding of paroxetine to the binding site induces a conformational change in the molecular complex of the binding site, whereas the binding of imipramine takes place without conformational changes in the binding site.

Binding Sites↗
PubMed1983

High affinity binding of [3H]paroxetine and [3H]imipramine to human platelet membranes.

Paroxetine, one of the most potent and specific serotonin uptake inhibitors, was tritiated and used for binding studies with human platelet membranes. Specific, high affinity binding was demonstrated. The binding was compared with [3H]imipramine binding; it was found that the maximal binding (Bmax) was the same for [3H]paroxetine and [3H]imipramine, whereas the affinity was much higher for [3H]paroxetine (KD 0.08 nM and 0.56 nM for paroxetine and imipramine binding, respectively). IC50 was calculated for the inhibition of [3H]paroxetine and [3H]imipramine binding by a number of antidepressants; the corresponding Hill coefficients were also calculated.

Antidepressive Agents, Tricyclic↗
PubMed1983

Peptic ulcer complaints in lithium-treated and non-lithium-treated manic-depressive patients.

A possible protective effect of lithium against the occurrence of peptic ulcer complaints in manic-depressive patients, treated with lithium, was investigated. 167 manic-depressive patients, 91 in lithium treatment, 76 not in lithium treatment, were questioned about clinical symptoms of peptic ulcer. Thirteen of the lithium-treated and 23 of the non-lithium-treated patients reported symptoms of peptic ulcer. The difference was statistically significant. The hypothesis that lithium treatment reduces the frequency of symptoms of peptic ulcer in manic-depressive patients was thus confirmed.

Bipolar Disorder↗
PubMed1982

Lithium effects on rat brain glucose metabolism in vivo. Effects after administration of lithium by various routes.

The effects of lithium on several brain energy metabolites were investigated in rats. Lithium was administered by three alternative routes: 1) in food, 2) via IP injection, or 3) intracisternally via the suboccipital route. Lithium given in food induced permanent changes, mainly in glycolytic processes and in glycogen content. Lithium injected IP induced, in addition, several changes which depended on the increase in brain lithium concentration following injection of lithium. These changes in brain metabolites disappeared as brain lithium concentration stabilized. Intracisternal injection of lithium produced brain lithium concentrations between 1 and 2 mmoles/kg wet wt., with a mean of about 1.6 mmoles/kg wet wt. Lithium concentrations below about 1.6 mmoles/kg wet wt. induced changes in brain metabolites which were similar to the changes seen after IP injection of lithium. Lithium concentrations above about 1.6 mmoles/kg wet wt. induced changes in several brain metabolites which were at variance with the changes induced by lower lithium concentrations. These changes were in many respects similar to changes in brain metabolites seen in rats exposed to convulsive treatment. It is hypothesized that such metabolic changes during lithium treatment, in discrete areas of the brain with higher concentration of lithium, e.g., hypothalamus, might be related to the prophylactic effect of lithium treatment in man.

Animals↗
PubMed1982

Lithium treatment regimen and renal water handling: the significance of dosage pattern and tablet type examined through comparison of results from two clinics with different treatment regimens.

For many year two Danish psychiatric hospitals having used different lithium treatment regimens. In one, slow-release tablets were given in two daily doses and, in the other conventional tablets were given in a single daily dose. In both hospitals many patients developed polyuria. Multiple regression analyses with sex, age, treatment duration, serum lithium concentration, and treatment regimen as predictor variables showed that the two treatment regimens did not affect the glomerular filtration rate or the proximal reabsorption differently, but that distal water reabsorption was significantly less affected and polyuria less pronounced in the patients given conventional tablets once daily than in those give slow-release tablets twice daily. The authors are divided among themselves as regards the implications of these findings.

Adult↗
PubMed1982

3H-Imipramine high-affinity binding sites in rat brain. Effects of imipramine and lithium.

The specific high-affinity binding of 3H-imipramine to rat brain membranes was investigated. Five weeks of lithium treatment decreased the number of binding sites, but had no effect on the affinity constants. Long-term imipramine treatment had no effect on the number of binding sites but apparently decreased the affinity. The latter effect was probably due to imipramine remaining in the membrane preparation.

Animals↗
PubMed1982

Lithium treatment: does the kidney prefer one daily dose instead of two?

Renal structure and function were investigated in two groups of long-term lithium treated patients. Lithium was administered in two different ways either in a one-dose per day schedule where the whole dose of lithium was given between 8 and 10 p.m. or in a schedule where the lithium dose was given, divided into two or three doses, during the day. Kidney biopsy was performed, and structural changes in the kidney tissue were determined together with 24-h urine volume in the individual patients. The functional as well as the structural changes were most pronounced in patients given their lithium in divided doses during the day. Lithium may be more harmful to the kidney when the lithium administration gives a relatively constant serum lithium level than when the administration causes greater variations including peak values and low minimum levels in serum lithium. The reason for this might be that a number of regenerative processes only occur in periods with low lithium concentrations.

Adult↗
PubMed1982

Lithium effects on calcium, magnesium and phosphate in man: effects on balance, bone mineral content, faecal and urinary excretion.

Calcium, magnesium and phosphate metabolism was studied in lithium-treated patients, using a metabolic balance technique. Two groups of patients participated in the study: 1) Patients who were to start on a prophylactic lithium treatment, and 2) Long-term lithium-treated patients whose treatment was to be terminated. Lithium treatment produced a positive balance in both calcium, phosphate and magnesium. By continuous lithium treatment the effect on magnesium wore off, whereas the effect on calcium and phosphate persisted. In urine, lithium induced a decrease in both calcium and phosphate excretion, whereas the excretion of magnesium was increased. Bone mineral content was measured by photon absorption, and lithium treatment resulted in a decrease in bone mineral content occurring within the first 6 months of lithium treatment. In the patients, bioavailability of the Li2CO3 preparation was found to be about 95%, and the patients contained about one 24-h dose of lithium just before the next dose of lithium was administered.

Biological Availability↗
PubMed1981

Functional and structural rat kidney changes caused by peroral or parenteral lithium treatment.

Renal functional and structural changes were studied in rats treated with lithium for 5 months. The lithium was administered in two different ways: in the food or as a daily intraperitoneal injection. In the perorally treated rats serum lithium was relatively constant during the day. In the injected rats serum lithium reached a high peak value just after the injection followed by a decrease to very low values. In all rats an increased water consumption and a reduced renal concentration ability were seen during lithium treatment. Light microscopy showed focal degenerative changes in the distal convoluted tubule and collecting ducts. These changes comprised nuclear and cellular polymorphism and tubular dilatation. The functional as well as the structural changes were most pronounced in the rats treated with peroral lithium, and a correlation between the functional and morphological changes was present. It is concluded that lithium is more harmful to the kidney when the administrations give a relatively constant serum lithium level, such as in peroral administration, than when administration causes great variations, including peak values and very low minimum levels in serum lithium. The reason for this might be that a number of regenerative processes occur only in periods with low lithium concentrations.

Administration, Oral↗