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PubMed1979

Differential antagonism of antiavoidance, cataleptic and ptotic effects of neuroleptics by biperiden.

The interaction between neuroleptics and an anticholinergic, biperiden, in the antiavoidance, catalepsy and ptosis tests was investigated in mice for the purpose of predicting the extrapyramidal side-effects of neuroleptics. The cataleptic effect of most neuroleptics used was antagonized to some extent by biperiden, while the ptotic effect was hardly influenced. The antiavoidance effect of haloperidol, trifluperidol and perphenazine was markedly antagonized and that of chlorpromazine moderately. However, the effect of thioridazine, chlorprothixene, levomepromazine and clozapine was little antagonized. In neuropharmacological tests, haloperidol, trifluperidol and perphenazine exhibited a selective antidopaminergic activity, while chlorprothixene, levomepromazine and clozapine showed antidopaminergic, antiadrenergic and also anticholinergic activities when similar doses were given. These results indicate that biperiden antagonism may be marked in the tests related to the extrapyramidal symptoms and in drugs liable to induce extrapyramidal side effects, however, there would be little or no antagonism in drugs possessing the anticholinergic property and eliciting few extrapyramidal side-effects.

Animals↗
PubMed1997

[A case of depression manifesting incessant pacing and wandering following discontinuation of antipsychotic drugs due to neuroleptic malignant syndrome: a possible involvement of withdrawal akathisia].

A depressed 36-year-old woman manifesting a delusion of persecution was started on neuroleptics. In parallel with the increase of neuroleptics, she suffered from akathisia, such as wandering, and thereafter developed neuroleptic malignant syndrome. Thus, neuroleptics were discontinued. As a result, she manifested severer wandering, impairment of conversation, and unacceptable behavior (e.g. touching her stool) though neuroleptic malignant syndrome subsided. These symptoms improved following the administration of levomepromazine and amitriptyline. It seems difficult to regard these symptoms as just a prolongation of akathisia, since the level and frequency of akathisia increased. It also seems unlikely to regard these symptoms as those of agitated depression, since there were no complaints of irritability. On the other hand, it seems probable that "withdrawal akathisia" occurred following the discontinuation of neuroleptics and the reinstituted levomepromazine improved the withdrawal phenomena consisting of severer wandering, impairment of conversation, and unacceptable behavior.

Adult↗
PubMed1999

Evaluation of Tiletamine-Zolazepam as an Anesthetic in Quail (Coturnix coturnix japonica).

The objective of the present study was to evaluate the effects of tiletamine-zolazepam (TZ) administered alone or in combination with atropine, xylazine, and levomepromazine to quail (Coturnix coturnix japonica). The induction time, duration of hypnosis and anesthesia, and time to recovery were determined. The presence or absence of tremor, upper respiratory tract secretions, and excitability and the degree of muscular tone were also observed. The results showed that doses from 10 to 100 mg/kg TZ administered alone or in combination with xylazine or levomepromazine failed to produce anesthesia; only hypnosis was obtained in a dose-dependent manner. Immediately after injection of the drug, histopathologic examination of the site of drug injection indicated the presence of discrete acute focal myositis. After 21 days, a discrete fibrosis between muscle fibers was detected in the pectoral muscle as a sign of scarring. We conclude that the administration of TZ to a dose of 100 mg/kg does not produce anesthesia in quail. For noninvasive and minimally painful procedures requiring chemical restraint and recumbency, the recommended dose is 30 mg/kg.

Journal Article↗
PubMed1990

[Phenothiazine-induced pseudolymphoma].

A 59-year-old male patient developed lymphoma-like cutaneous infiltrates on the back and left side following treatment with levomepromazine (Neurocil) over many years. Complete remission after discontinuation of levomepromazine and its replacement by a drug of another chemical class (melperone, Eunerpan) confirmed the causative role of the phenothiazine in the development of pseudolymphoma.

B-Lymphocytes↗
PubMedDate not supplied

[The effect of antidepressants on the experimental anticonvulsant activity and acute toxicity of anticonvulsants].

In the experiments on white mice there was studied the anticonvulsant activity by the test of the maximal electric shock and acute toxicity of anticonvulsants and antidepressants at separate and combined administration. The combined use of anticonvulsants and antidepressants showed the increase of the anticonvulsant activity of phenobarbital with amitriptyline, levomepromazine and lithium oxybutyrate; diphenine and carbamazepine with amitriptyline as well as hexamidine with all antidepressants. The combination of phenobarbital with amitriptyline, levomepromazine and lithium oxybutyrate, diphenine with amitriptyline, hexamidine with amitriptyline and imizine proved to be the safest.

Animals↗
PubMed1977

Studies on antituberculotic action of some phenothiazine derivatives in vitro.

Five phenothiazine derivatives (chlorpromazine, levomepromazine, diethazine, promethazine and chlorpromazine) sulphoxyde were tested for antimycobacterial activity. The growth of Mycobacterium tuberculosis, M. bovis and M. butyricum was inhibited by chlorpromazine practically at identical concentrations. The minimum inhibitory concentrations for M. tuberculosis were: chlorpromazine and levomepromazine, 10 microgram/ml; diethazine and promethazine 20 microgram/ml, whilst chlorpromazine sulphoxyde was ineffective even at a concentration of 100 microgram/ml. Chlorpromazine and promethazine exerted a measurable bactericidal activity on M. tuberculosis at 50 microgram/ml; total destruction of the organism and loss of acid fastness in part of the cells were shown at 300 microgram/ml. Preliminary studies, in mouse experiments phenothiazine derivatives were ineffective.

Antipsychotic Agents↗
PubMed1978

[Lithium modifications of the cataleptogenic properties of various neuroleptic drugs in the rat].

After unique ip injection (11,78 mEq/kg) LiCl increases in the Rat catalepsy produced by chlorpromazine, prochlorperazine, fluphenazine, levomepromazine, haloperidol and reserpine. This phenomenon is more important according to cataleptigenic properties of neuroleptic drugs. After repeated injections of LiCl (5 mEq/kg/d/5 dip) potentiation of catalepsy is more fugacious and not produced by levomepromazine and reserpine. LiCl would interfere at enzymatic level with dopaminergic transmission either by inhibiting activity of cerebral adenylcyclase (unique injection) or by inhibiting dopamine synthesis (repeated injections).

Animals↗
PubMedDate not supplied

[Effect of phenothiazine derivatives on the development of experimental traumatic brain edema].

The effect of levomepromazin, propazin, diprazin and dyphenhydramine on the development of traumatic edema of the brain has been studied. Phenothiazine derivatives with an unbranched dialkylaminoalkyl side chain at the nitrogen atom (propazin) have been found to produce the most remarkable antiedematic action. The drugs that have a branched dialkylaminoalkyl chain (levomepromazin, diprazin) do not return brain water content to normal.

Animals↗
PubMed1993

Replacement of chlorpromazine with other neuroleptics: effect on abnormal skin pigmentation and ocular changes.

This paper describes the outcome of 15 patients with chlorpromazine (CPZ)-induced abnormal skin pigmentation (ASP) in whom CPZ was replaced with other neuroleptics for three to 13 years. Complete resolution of ASP occurred over a period of six months to five years following substitution with haloperidol (four patients), levomepromazine (three patients), trifluoperazine (one patient), thioproperazine (one patient) as the sole neuroleptic, by a combination of two of the three phenothiazines (four patients) or haloperidol plus pipotiazine (one patient). Resolution was maintained during the remainder of the follow-up period. In one patient, at final follow-up, marked improvement was present three years after CPZ was replaced with levomepromazine. Bilateral lenticular pigmentary deposits persisted in all eight patients examined 3.3 to 13 years after replacing CPZ and less than three months to nine years after resolution of ASP; improvement was noted in only one of these patients. Bilateral endothelial corneal deposits, present in five patients while on CPZ therapy, had disappeared in two patients seven and 13 years, respectively, after replacing CPZ; improvement was noted in two other patients. These findings indicate that: 1. CPZ-induced ASP is completely reversible in most, if not all, patients if CPZ is withdrawn; 2. a variety of neuroleptics including other phenothiazines can be used to replace CPZ without risk of re-emergence of ASP; 3. CPZ-induced lenticular changes persist whereas corneal changes may resolve slowly over a period of many years following replacement of CPZ; 4. ASP and ocular changes induced by CPZ may be subserved by two different pathophysiological mechanisms.

Adult↗
PubMed1976

[Microbiological assay of some phenothiazine derivatives using different strains of Bacillus subtilis].

This paper deals with the microbiological assay of chloropromazine, levomepromazine and promethazine, whose bacteriostatic power was measured in the diffusion test against four different strains of Bacillus subtilis. The four strains proved to be equally sensitive to solutions of phenothiazine derivatives containing more than 0.5 mg/ml. There was no difference between the four strains as referred to the median percentual error in the chlorpromazine determination. The median percentual error has been very high (around 20%) in the levomepromazine determination using Bacillus subtilis ATCC 9945. When promethazine was used against the four strains of Bacillus subtilis a very high percentual error (around 20%) has been obtained, therefore, they are not recommended for the promethazine determination.

Bacillus subtilis↗
PubMed1993

[A case of life-threatening ventricular arrhythmias probably due to psychotropic drugs].

We present a case provoked life-threatening ventricular arrhythmias probably due to psychotropic drugs. The patient was a 55-year-old man who had previously twice operations of aortic valve replacement (AVR). The signs of cardiac failure were recurrently appeared from the end of 1991, and he had received promethazine and sulpiride for his depressive state. From cardiac catheterization, we planned his third AVR. The electrocardiographic (ECG) QTc interval was prolonged to 0.48 seconds on this admission. In March 1992 syncopal attack appeared suddenly, and his monitor ECG revealed frequent polymorphous ventricular tachycardia (VT) and Torsade de Pointes (Tdp). These arrhythmias stopped by emergent cardiac pacing. After discontinuing these psychotropic drugs, no ventricular arrhythmias appeared. Since the patient complained severe insomnia one month before operation, the diminished dose of psychotropic drugs (promethazine and levomepromazine) was readministered. Ten days after the operation, syncopal attack reappeared and his ECG recorded frequent VT and Tdp. During both syncopal attacks his serum potassium and magnesium were within normal limits. Two days later, he died from multi-organ failure. We concluded that life-threatening arrhythmias such as VT and Tdp might develop under the administration of mild psychotropic drugs (promethazine or levomepromazine), therefore, must better take a care of ECG changes in cases of using any psychotropic drugs.

Electrocardiography, Ambulatory↗
PubMed1997

Plasma concentrations of antipsychotic drugs in psychiatric inpatients.

In current psychiatric therapy, two or more kinds of antipsychotic drugs are usually prescribed in Japan. However, there are few data on the therapeutic plasma concentrations of antipsychotic drugs or on the correlation between the daily dose and the plasma concentration, in cases where several antipsychotic drugs had been prescribed for each patient. We measured the therapeutic plasma concentrations of 9 antipsychotic drugs in 24 psychiatric inpatients during a 6-month period. They were treated with fixed dosages of antipsychotic drugs. Plasma samples were collected early in the morning once a month, and the concentrations of antipsychotic drugs were determined by gas chromatography with nitrogen phosphorus detection, high-performance liquid chromatography (HPLC) with fluorescence detection and HPLC with UV detection. The plasma levels of chlorpromazine, levomepromazine, thioridazine, haloperidol, bromperidol, zotepine, oxypertine, sulpiride and sultopride were 21.8-92.4, 31.7-156, 101-203, 16.4-56.2, 2.72-11.7, 13.6-84.0, 29.9-80.4, 70.1-1,120 and 35.7-2,990 ng/ml, respectively. A linear correlation between the daily dose and the plasma concentration was noted for sultopride, levomepromazine, sulpiride, haloperidol, chlorpromazine and zotepine.

Adult↗
PubMed1992

Structural changes by sulfoxidation of phenothiazine drugs.

The side-chain conformations of psychoactive phenothiazine drugs in crystals are different from those of biologically inactive ring sulfoxide metabolites. This study examines the potential energies, molecular conformations and electrostatic potentials in chlorpromazine, levomepromazine (methotrimeprazine), their sulfoxide metabolites and methoxypromazine. The purpose of the study was to examine the significance of the different crystal conformations of active and inactive phenothiazine derivatives, and to determine why phenothiazine drugs lose most of their biological activity by sulfoxidation. Quantum mechanics and molecular mechanics calculations demonstrated that conformations with the side chain folded over the ring structure had lowest potential energy in vacuo, both in the drugs and in the sulfoxide metabolites. In the sulfoxides, side chain conformations corresponding to the crystal structure of chlorpromazine sulfoxide were characterized by stronger negative electrostatic potentials around the ring system than in the parent drugs. This may weaken the electrostatic interaction of sulfoxide metabolites with negatively charged domains in dopamine receptors, and cause the sulfoxides to be virtually inactive in dopamine receptor binding and related pharmacological tests.

Antipsychotic Agents↗
PubMed1975

[Plasma levels of imipramine and desmethylimipramine and antidepressant effect during controlled therapy(author's transl)].

24 depressed impatients received a standardized treatment by imipramine, 6 among them receiving also levomepromazine. Plasma concentration of imipramine and DMI were controlled weekly during the study, and standardized assessment of clinical state were made by a psychiatrist who was unware of biochemical findings. Interaction between the antidepressant and neuroleptic metabolism is shown by a significant increase of DMI levels, though the clinical effect of the drug association could not be asserted. The therapeutic effect seems mainly dependant of etiology of depression. Endogeneous depressions improve more than other types. Among endogenous depressions a significant correlation was found between the degree of clinical improvement after three weeks and DMI level, sum of imipramine + DMI level, but not with concentration of imipramine alone.

Adjustment Disorders↗
PubMed1983

Pharmacological characterization of the receptors involved in the apomorphine-induced polyphasic modifications of locomotor activity in mice.

Increasing doses of apomorphine elicited polyphasic changes in locomotor activity in mice, consisting of: (i) hypokinesia with a peak effect at 25 micrograms/kg, which was not antagonized by various neuroleptics used at the highest doses not changing spontaneous locomotor activity, except for haloperidol; (ii) a relative restoration of locomotor activity at 75 micrograms/kg; this effect was antagonized by all the neuroleptics tested (except clozapine) and was hardly affected by domperidone and sulpiride; this apomorphine-induced effect was markedly increased 12 days after ICV 6-hydroxydopamine, (iii) a further hypokinetic effect with a peak effect at 150 micrograms/kg-1 (occurring simultaneously with hypothermia) which was antagonized by all the neuroleptics tested (including sulpiride at low doses) except levomepromazine and clozapine, and was again hardly affected by domperidone; this hypokinesia was reduced after prior (24 h) administration of 5 mg/kg apomorphine, (iv) finally another restoration of locomotor activity was observed at doses of apomorphine above 200 micrograms/kg.

Animals↗
PubMed1983

Combined treatment of tardive dyskinesia with clonidine and neuroleptics: a follow-up study of three cases for three years.

Three cases of tardive dyskinesia with psychotic symptoms (one presenile psychosis; two schizophrenia) were successfully treated with both clonidine and neuroleptics for 3 years. The dyskinesia abolished or reduced by clonidine returned several months after discontinuation of clonidine. During the follow-up study, it was observed that combining neuroleptics with clonidine was superior to thioridazine, levomepromazine, or sulpiride for controlling the dyskinesia. These findings suggest that noradrenergic involvement is important in tardive dyskinesia and that other subtypes of dyskinesia might exist.

Antipsychotic Agents↗
PubMed1986

Steady-state levels of imipramine and its metabolites: significance of dose-dependent kinetics.

Seventeen hospitalized patients (age 39-66 years), received a loading dose of 100 mg imipramine HCl and then 50 mg b.i.d. The 12-h plasma concentration at steady-state varied between 40-637 nmol/l for imipramine, 49-1148 nmol/l for desipramine and 89-1603 nmol/l for imipramine + desipramine. Guided by plasma level monitoring, a final therapeutic plasma level between 548-910 nmol/l for imipramine + desipramine was achieved (therapeutic dose range: 50-400 mg/day). Mean time to reach the therapeutic level was 19 days. The mean 2-OH-imipramine/imipramine ratio was 0.24 and mean 2-OH-desipramine/desipramine ratio was 0.56. There was a significant intrapatient correlation between the two ratios, both during 100 mg imipramine/d and at the therapeutic dose level. A low ratio was associated with high imipramine and particularly with a high desipramine level. Well defined steady state levels were established at two different dose levels in 12 patients and at three dose levels in 5 patients. With increasing dose there was a marked and disproportionate rise in the desipramine level and to some extent in the imipramine level. Saturation of imipramine and desipramine hydroxylation appeared to be responsible for the dose-dependent kinetics. Concomitant treatment with levomepromazine and perphenazine in one patient resulted in a significant rise both in imipramine and desipramine concentration, apparently due to inhibition of the hydroxylation. Eleven out of twelve endogenously depressed patients responded completely to treatment, whereas the response was poor in the non-endogenously depressed patients despite optimal drug levels.

Adult↗