PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “METHOTRIMEPRAZINE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 757 records · Page 42Linked to original sources
PubMedDate not supplied

[Acute catatonia and neuroleptic malignant syndrome. A case of infantile psychosis].

Similar clinical and biological features in lethal catatonia (LC) and neuroleptic malignant syndrome (NMS) suggest a relationship between both affections and common physiopathologic mechanisms. Pharmacological effects of several drugs--dopaminergic agonists, benzodiazepines, carbamazepine--suggest an impairment of several systems of neurotransmitters. We report the case of a young woman with infantile psychosis who developed catatonic syndrome worsened by neuroleptic treatment, arising the problem of the chronology of both affections. The evolution with treatment may partially explain the physiopathology. A 18-year old woman with an history of infantile psychosis, experienced insomnia, anorexia, paradoxical agitation developed after affective traumatism (mother's hospitalization). Chlorazepate (150 mg) remained inefficient and hospitalization was necessary. The patient was dumb, prostate in bed. She presented negativism, rigidity of the four limbs, catalepsia and hyperpyrexia (38.5 degrees C). Hepatic transaminases were increased (SGOT: 71 UI/l; N < 30). After cumulated dose of levomepromazine (100 mg) profuse sudation, thermic and cardiovascular instability, alteration of consciousness, major rigidity of limbs appeared. (Blood) hepatic transaminases and muscular enzymes increased. Bacteriological samples, cerebrospinal fluid analysis, CT-scan and EEG were normal. Within 48 hours after rehydratation and bromocriptine (30 mg per day) alteration of consciousness and autonomic disorders decreased but hyperpyrexia (38 degrees C) persisted. Biological parameters were normalized 10 days later. Negativism and psychomotor inertia remained. Lorazepam (3 mg per day) failed to be clinically beneficial. On carbamazepine (600 mg per day) she started speaking and moving spontaneously. Catalepsia disappeared but rigidity and anorexia persisted. Electroconvulsivotherapy (ECT) was necessary. After 2 shocks she started standing up, walking, taking food and speaking fluently.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1976

Antibacterial effect of some phenothiazine compounds and R-factor elimination by chlorpromazine.

Chlorpromazine, levopromazine and promethazine exerted a bacteriostatic effect on Gram-positive bacteria at 20-60 mug/ml, on Gram-negative bacteria at 130-180 mug/ml concentration. Of the three compounds, chlorpromazine had the most marked bactericidal effect on cultures of Bacillus anthracis growing in minimal medium. In addition, chlorpromazine had a significant bactericidal effect on the resting cells of Escherichia coli suspended in saline. Pseudomonas aeruginosa was resistant to phenothiazines. Experiments have failed to derive resistant mutants from the highly sensitive B. anthracis. An effective R-factor elimination was observed at chlorpromazine concentrations of 50 mug/ml, practically not affecting the growth of multiple resistant E. coli.

Bacillus anthracis↗
PubMed1993

Effects of the combination of ketoconazole and calmodulin inhibitors against Candida albicans in vitro. Short communication.

The susceptibility of 66 strains of Candida albicans from patients was tested against ketoconazole (Ktz), chlorpromazine (Chl) levomepromazine (Lev), haloperidol (Hal) and the combination of Ktz with these calmodulin inhibitors, using Sabouraud's broth. The minimal inhibitory concentrations (MICs) for 66 strains of C. albicans were as follows: Chl 192 +/- 11.4 micrograms/ml, Lev 306 +/- 16.4 micrograms/ml, Hal 464 +/- 13.8 micrograms/ml compared with Ktz 34.46 +/- 3.9 micrograms/ml. The combination of Ktz and calmodulin inhibitors in various ratios (1:1,1:2,2:1) was found to exert synergistic effect and the mean values of the combinations were: Ktz+Chl 3.45 +/- 0.35, 3.78 + 0.36, 5.58 + 0.4 micrograms/ml; Ktz+Lev 10.8 +/- 2.19, 9.7 +/- 2.23, 10.5 + 2 micrograms/ml; Ktz+Hal 6.4 +/- 1.7, 6.8 +/- 1.6, 7.28 +/- 1.5 micrograms/ml. These results were significantly different (p < 0.001) from those of ketoconazole. These findings indicate that some calmodulin inhibitors increase the antifungal activity of Ktz against C. albicans in vitro.

Calmodulin↗
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↗
PubMedDate not supplied

[The effect of phenothiazine derivatives that inhibit glucocorticoid receptor function on the state of the renin-angiotensin system].

Aminazine, 30 mg/kg, and tisercin, 30 mg/kg, were tested for their effects on the activities of angiotensin-converting enzyme (ACE), renin and the levels of aldosterone. Blood and lungs were taken 1 and 24 hours after intraperitoneal administration of the drugs to male rats. Tisercin was found to inhibit the activity of ACE and enhanced that of renin and elevated the levels of aldosterone in the serum and lung cytosol 24 hours following the agent administration. Aminazine depressed the activity of ACE and increased the serum levels of aldosterone 1 and 24 hours post-administration.

Aldosterone↗
PubMed1993

Citalopram: interaction studies with levomepromazine, imipramine, and lithium.

The pharmacokinetic interactions between the selective serotonin reuptake inhibitor citalopram, given as an oral dose of 40 mg/day for 10 days, and (1) levomepromazine (50 mg single oral dose), (2) imipramine (100 mg single oral dose), and (3) lithium (30 mmol/day orally for 5 days) were examined in three panels each of 8 healthy young male volunteers (age 20-31). All volunteers were classified as extensive metabolizers of sparteine and mephenytoin. Each subject completed three study phases--one with citalopram alone, one with one of the three other drugs, alone, and one with citalopram combined with the corresponding other drug. For citalopram and its metabolites, a non-enantioselective analytical method (high-performance liquid chromatography) was used. Only two statistically significant interactions were indicated. First, levomepromazine caused a 10-20% increase from the initial steady-state levels of the primary citalopram metabolite, desmethylcitalopram. Second, citalopram caused approximately 50% increase in the single-dose area under the serum concentration/time curve of desipramine (primary metabolite or imipramine) and a corresponding reduction in the level of the subsequently formed metabolite 2-hydroxydesipramine. These findings are in agreement with the recent observations that (1) the demethylation of desmethylcitalopram (to didesmethylcytalopram) is partly mediated via the sparteine/debrisoquine oxygenase (CYP2D6) and that levomepromazine is a potent inhibitor of CYP2D6, and (2) that desmethylcitalopram has a somewhat stronger affinity for CYP2D6 than desipramine, and therefore may inhibit the hydroxylation of desipramine, which is also a substrate of CYP2D6.

Adult↗
PubMed1977

Influence of the antiparkinsonian drugs on the plasma level of neuroleptics.

The interaction between various neuroleptics and antiparkinsonian drugs was analyzed by measuring the neuroleptic plasma level before and after withdrawal of antiparkinsonian drugs. The population completing the study consisted of 32 chronic schizophrenics treated with chlorpromazine (8), levomepromazine (14), thioridazine (6), or haloperidol (4). Twenty-five were also receiving benztropine; 4, trihexyphenidyl; and 3, procyclidine. During the first 4 weeks patients remained on neuroleptics and antiparkinsonians, the latter being withdrawn during the 5th week, and the neuroleptics alone being administered during 16 following weeks. The plasma level of neuroleptics was assayed by gas liquid chromatography, once weekly in the morning at two different times. The analysis of variance showed a significant difference in neuroleptic plasma level when patients took neuroleptics only versus the period they had received neuroleptics and antiparkinsonians. The multiple comparison based on Studentized range Q0-05 revealed a significant progressive increase of neuroleptic plasma level during 12 weeks after withdrawal of antiparkinsonian drugs after which a plateau was reached. The hypothetical mechanisms of action of antiparkinsonians on neuroleptic plasma level are discussed.

Adult↗
PubMed1995

Bioequivalence and absolute bioavailability of oblong and coated levomepromazine tablets in CYP2D6 phenotyped subjects.

The bioequivalence and absolute bioavailability of oblong and coated levomepromazine tablets were studied in 12 healthy volunteers. A 1-hour intravenous infusion served as the reference. Serum concentrations of levomepromazine were quantified with a specific high-performance liquid chromatographic method and electrochemical detection. The 2 oral formulations were bioequivalent. After oral administration of oblong and coated levomepromazine tablets the mean serum concentration versus time profiles were similar and the pharmacokinetic parameters showed wide interindividual variations. There was a 21% absolute bioavailability of levomepromazine, indicating a pronounced presystemic metabolism. The total serum clearance and the apparent volume of distribution at steady state were 48 +/- 14 l/min and 980 +/- 213 l, respectively. These pharmacokinetic parameters were also investigated with respect to the CYP2D6 polymorphism, i.e. via dextromethorphan phenotyping of 9 subjects, 3 subjects were poor metabolizers, and 6 extensive metabolizers. The Spearman's rank-ordered correlation analysis did not reveal a significant correlation between the pharmacokinetic parameters AUC, Cmax and t1/2 after oral administration of oblong and coated levomepromazine tablets and the metabolic ratios of dextromethorphan, suggesting that levomepromazine is not metabolized to any major extent by the isoenzyme CYP2D6.

Administration, Oral↗
PubMed1996

[A case of malignant neuroleptic syndrome. Case report].

We report on a woman patient with organophosphate poisoning resulting from a psychotically motivated suicide attempt. After detoxification and during treatment with haloperidol and levomepromazine, she developed acute malignant neuroleptic syndrome (MNS) in which dyspnea requiring assisted ventilation was the main symptom. Discontinuation of the neuroleptics was enough to effect sufficient recovery. With this case report, we would first like to emphasize that MNS can evolve within a very short time into a severe and life-threatening situation requiring intensive medical care, and secondly to illustrate the implications of organophosphate poisoning and the consequent cholinesterase blocking far the differential diagnosis of MNS.

Adult↗
PubMed1998

[A study of neuroleptic malignant syndrome in the presenium and senium].

Recently, with the increase in elderly population, we have had more opportunities to administer neuroleptics to elderly patients for hallucinatory delusional state, delirium, psychomotor excitement, wandering etc. However, little is known about the characteristics of the neuroleptic malignant syndrome (NMS) in elderly patients, which is the most serious side effect of neuroleptics. In this paper, we present the clinical course of five NMS patients in the presenium and senium. Case 1 was 72-year-old male who was diagnosed as having dementia of Alzheimer's type (with late onset). He showed nocturnal wandering, insomnia, and irritability. Tiapride 60 mg per day had been administered previously. Just after the addition of oxypertine 10 mg per day, NMS occurred, and he died of pneumonia a week later. Case 2 was 75-year-old male who was diagnosed as having vascular dementia. He showed insomnia, hyperactivity and wandering. He had been given levomepromazine (LPZ) 10 mg per day over a long period of time. At first, he had daily episodic fever, however, serum CPK levels did not increase at that time. A month later, all the symptoms of NMS appeared and then the patient's condition suddenly deteriorated and he died three days later. Case 3 was a 64-year-old male who was diagnosed as having dementia of Alzheimer's type (with early onset). He showed insomnia, irritability and violence. Tiapride 50-125 mg per day was administered along with oxypertine 50-115 mg per day. Almost two months later, NMS occurred. He had daily episodic fever at first, extrapyramidal symptoms and autonomic instabilities gradually increased. Soon after symptoms of NMS were completed. In this case, NMS seemed to be induced by bacterial pneumonia after long term administration of LPZ 5 mg per day. Case 4 was a 75-year-old female who was diagnosed as having dementia of Alzheimer's type (with late onset). She showed hallucinatory delusional state. Although she had autonomic instabilities just after adminstration of haloperidol 1-2 mg per day, NMS itself occurred after discontinuing the neuroleptic. Case 5 was a 61-year-old female who was diagnosed as having schizophrenia at the age of forty. She was given various neuroleptics over a period of time. The neuroimaging in SPECT showed her cerebral cortex was generally hypoactive. She had a tendency to have autonomic instabilities after the administration of relatively high potential neuroleptics. Risperidone 3-6 mg per day was administered, and almost a month later, autonomic instabilities increased and she was diagnosed as having NMS. All the patients would be able to have brain dysfunction, which suggested that such patients may be liable to NMS. In our patients, NMS occurred after the additional administration of oxypertine 10 mg per day or after long time administration of LPZ 5 mg per day. It was suggested that NMS could occur after the administration of low dose and relatively low potential neuroleptics in elderly patients. Our 3 of 5 patients showed the delayed type of NMS, which might be relatively more frequent in senior and presenior patients than in younger patients. In case 3, NMS was induced by the somatic disease (bacterial pneumonia), however in other cases, NMS was not always induced by somatic disease. Our 4 of 5 patients experienced some of the symptoms of NMS--episodic fever, extrapyramidal symptoms and autonomic instabilities--before the onset of NMS. Such symptoms may be "pre-steps" to NMS. Once NMS occurred, the patient's systemic condition tended to deteriorate acutely. Due to the fact that our 2 of 5 patients died, it was suggested that the prognosis of the NMS patients in presenium and senium tends to be much worse. It is important to find the "pre-steps" to NMS and treat them as soon as possible for better prognosis.

Aged↗
PubMed1976

[Anesthetic technics for surgery in otoneurology].

A description is given of a technique named "Protected Sleep", which produces a deep and residual analgesia and neurolepsia, without interfering with spontaneous respiration. A deep, stable and reliable neuroanesthesia is achieved by means of a partial pharmacodynamic blockage of the neuro-humoral reaction system. It is recognisable by the following features: 1 degree a smooth transition through pre-, per- and post-operative stages, avoiding in particular immediate awakening; 2 degrees a relative arterial hypotension, low venous pressure good peripheral circulation and tissular perfusion; 3 degrees light hypothermia; 4 degrees completely spontaneous respiration. This last factor is, to our way of thinking, of great importance: The venous return remains physiologically unchanged during inspiration in the peroperative as well as in the pre- and postoperative phases, enabling the maintenance of a constant, low venous pressure. Furthermore, should danger exist, the preservation of spontaneous respiration facilitates the immediate control of the respiratory centre. In this way we can obtain: 1. An almost perfect bloodless surgical field with good conditions for dissecting. 2. A low cerebro-spinal fluid pressure. 3. Decreased brain volume. 4. Absence of postoperative haemorrage. 5. Little of no postoperative oedema. 6. Little or no postoperative hyperthermia. "Protected sleep" is a pharmacodynamic technique realised mainly through administration of a combined and sufficient dose of pethidine, N-allyl-normorphine and levome promazine. For induction, a given dose of diazepam is combined with a single dose of succinyl-choline, to facilitate intubation, followed by a large dose of the narco-neuro-leptanalgesic mixture. For maintenance, nitrous oxide, oxygen, methoxyflurane and additional doses of the mentioned mixture are administered. Undirectional gas flow, without rebreathing, is provided, using the Ruben valve. In this paper on neuroanaesthesia, the technique of "Protected Sleep" and the pre-, per- and postoperative management and positioning of the neurosurgical patient are described in detail.

Anesthesia, General↗