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At least 19 recordsLinked to original sources
PubMed1976

Gas-liquid chromotographic determination of perazine, thioridazine and thioridazine metabolites in human plasma.

A gas-liquid chromatographic method for the detection of perazine, thioridazine and its major metabolites in human plasma is presented. Repeated extraction, an internal standard and a temperature program with flame ionization detection make possible accurate and reproducible results with patients on therapeutic doses of these drugs. Examples of chromatograms after extraction of plasma are given.

Antipsychotic Agents↗
PubMed1975

Thioridazine stimulates prolactin secretion in man.

Thioridazine, unlike most other effective antipsychotic drugs, appears to be only a weak dopamine antagonist in various regions of the brain. We decided to test, indirectly, thioridazine's effects on another brain dopaminergic system, the tuberoinfundibular tract, which regulates prolactin secretion by stimulating hypothalamic secretion of prolactin-inhibiting factor. Chlorpromazine and several other phenothiazines have been shown to stimulate prolactin secretion. Five healthy men ingested 50 mg of chlorpromazine concentrate on one occasion, and 50 mg of thioridazine concentrate on another. Both drugs noticeably stimulated prolactin secretion within two hours. It is concluded that thioridazine is a potent dopamine antagonist in the tuberoinfundibular system, and it is suggested that this system's regulation of prolactin secretion may provide a useful method for studying antipsychotic drug effects in man.

Administration, Oral↗
PubMed1979

Thioridazine and EKG anomalies.

Acute i.v. infusion but not daily oral administration of thioridazine-HCl in the dog produced EKG anomalies similar to those reported in psychiatric patients taking this drug. Lack of EKG effects after thioridazine-5-sulfoxide infusion and presence of anomalies after thioridazine at equivalent doses suggests further evaluation of the relationship between reported plasma levels of thioridazine and its ring-sulfoxide in association with EKG changes.

Animals↗
PubMed1977

Measurement of thioridazine in blood and urine.

1 Thioridazine can be specifically, simply, and reliably measured in plasma and urine by gas chromatography using hexane extraction and prochlorperazine as internal standard; fluorimetry is non-specific. 2 The method can also measure thioridazine ring sulphoxide, and mesoridazine-plus-sulphoridazine (M/S). 3 After single doses plasma sometimes shows M/S in addition to thioridazine itself; it always does so on continued treatment. There is great individual variation in both components, and evidence of changes in metabolism during the early weeks. 4 Urinary excretion may be influenced by pH, but between pH 6.0-7.0 about 1% of the daily dose appears in 24 h urine as the following: free thioridazine in microng quantities, M/S and ring sulphoxide each in mg amounts. 5 Patients attain steady state conditions, although plasma levels rise considerably after each dose and settle again in about 10 h. After chronic treatment is stopped to half-life is at about 30 h. 6 Plasma levels cannot be related to therapeutic response when this is slow, as in schizophrenia, but interpretations are complicated by the production of clinically active metabolites, and by plasma protein binding.

Chromatography, Gas↗
PubMed1979

Double-blind study of thioridazine and haloperidol in geriatric patients with a psychosis associated with organic brain syndrome.

Forty geriatric patients from the psychiatric ward of a state hospital were enrolled in a 12 week double-blind comparative study of the concentrate forms of thioridazine and haloperidol. The objective of the study was to assess the efficacy and safety of these drugs in the treatment of psychosis associated with organic brain syndrome in the elderly. Two types of patients comprised the population, those who had been hospitalized most of their adult lives and those who had not entered the hospital until late in life. Although both drugs produced significant improvement in these patients' symptoms, the improvement with thioridazine tended to be greater than that with haloperidol in most ratings. A plateau effect was seen with haloperidol in contrast to a steady improvement seen with thioridazine. The safety of both drugs was confirmed. Geriatric patients who display both psychotic and OBS symptomatology were found to respond quite well to both drugs, regardless of their previous psychiatric history, but a somewhat more dramatic response was seen with thioridazine.

Aged↗
PubMed1975

Effects of clozapine, thioridazine, perlapine and haloperidol on the metabolism of the biogenic amines in the brain of the rat.

The effects of clozapine, thioridazine, perlapine and haloperidol on the metabolism of the biogenic amines in the brain of the rat have been investigated. Haloperidol, perlapine and thioridazine induce catalepsy and enhance the turnover of DA in the striatum as indicated by the dose-dependent increase in the DA-metabolites, HVA and DOPAC. These effects are due to blockade of dopaminergic transmission, haloperidol being far more potent than perlapine or thiridazine. Clozapine differs from these agents in that it elevates the concentration of striatal DA. The increase of the concentrations of HVA and DOPAC by clozapine is not accompanied by development of catalepsy. Therefore, clozapine seems to influence striatal DA by a mechanism other than DA-receptor blockade. All four drugs enhance the turnover of NA in the brain stem. This effect is probably secondary to the blockade of NA-receptors. There was no correlation between the effects on NA-metabolism and the EEG-arousal inhibitory activities of these agents or their clinical antipsychotic effects. Clozapine increase the concentration of 5-HT and 5-HIAA in the brain. This effect was not seen with the other drugs. Perlapine seems to enhance the turnover of 5-HT, whereas haloperidol reduced the 5-HT concentration. Thioridazine appears to have no effect on the metabolism of 5-HT.

Animals↗
PubMed1979

Prolongation of the ejaculation latency in the male rat by thioridazine and chlorimipramine.

Thioridazine (3 mg/kg) and chlorimipramine (1.5-6.0 mg/kg) prolonged the ejaculation latency and increased the number of mounts but did not change the number of intromissions preceding ejaculation. Blockade of peripheral and central noradrenaline receptors by phentolamine and phenoxybenzamine respectively resulted in a suppression of all aspects of the sexual behavior with increasing doses. DL-5-HTP (25-100 mg/kg) in combination with an inhibitory of peripheral 5-HTP decarboxylase (benserazide, 25 mg/kg) produced, like chlorimipramine and thioridazine, a prolongation of ejactulation latency and an increase in the number of mounts preceding ejaculation. Selective inhibition of 5-HT reuptake however, by zimelidine (0-20 mg/kg) or alaproclate (0-20 mg/kg) did not affect the mating behavior. At higher doses of these drugs some animals failed to initiate sexual activities. There was an increase in the postejaculatory interval but not change in the ejaculatory latency. It is concluded tha the prolonged ejaculation latencies observed following treatment with thioridazine or chlorimipramine is not due to a blockade of central or peripheral adrenergic alpha-receptors.

5-Hydroxytryptophan↗
PubMed1979

Effects of thioridazine (Mellaril) on ventricular electrophysiologic properties.

The effects of therapeutic and toxic doses of thioridazine (Mellaril) (10 and 50 mg/kg body weight, respectively) on ventricular electrophysiologic properties were studied in 12 anesthetized dogs. Threshold pacing currents (diastolic threshold), effective refractory period and conduction time were significantly increased, and idioventricular automaticity was suppressed after administration of 10 mg/kg of thioridazine; the effects were much more pronounced after administration of 50 mg/kg. Rapidly repetitive responses or tachycardia could be induced in the ventricle by two early premature beats in 9 of the 12 dogs after the 50 mg/kg dose, but they did not occur before drug administration or after the 10 mg/kg dose. These results indicate that the antiarrhythmic and arrhythmogenic effects of thioridazine are dose-dependent and that careful monitoring with frequent electrocardiograms is needed for patients receiving large doses of this drug.

Animals↗
PubMed1979

Neurotoxicity with combined use of lithium and thioridazine.

Four cases on a combination of lithium and thioridazine developed severe neurotoxic symptoms, e.g., delirium, seizures, encephalopathy and grossly abnormal EEG's. All patients had been on lithium without thioridazine prior to and after the neurotoxic episode with no complications or EEG changes. The possible risk of combining lithium and neuroleptics (thioridazine) is discussed and repeated EEGs are recommended as a preventive measure.

Adult↗
PubMedDate not supplied

A controlled double-blind study of haloperidol versus thioridazine in the treatment of restless mentally subnormal patients. Serum levels and clinical effects.

A randomized cross-over trial was conducted in 30 restless mentally subnormal patients by increasing the dosage of haloperidol from 10 to 60 mg and of thioridazine from 100 to 600 mg daily. The effects of drug holidays and serum drug levels were also examined. Mesoridazine had 5-6 times higher serum levels than the parent compound and relatively high serum levels are achieved already with moderate doses. The observed differences between haloperidol and thioridazine treatment were surprisingly few. Serum cholesterol was higher (P < 0.05) at the end of the thioridazine administration. Drug holidays may benefit may patients.

Adolescent↗
PubMed1976

Psychomotor skills during subacute treatment with thioridazine and bromazepam, and their combined effects with alcohol.

Twenty paid healthy students volunteered for a doubleblind cross-over trial on the effects of two weeks' treatment with placebo, thioridazine and bromazepam on psychomotor skills. The doses used were thioridazine 10 mg t.i.d. during the first week and 20 mg t.i.d. during the second week, or 6 mg of bromazepam t.i.d. during two weeks choice reaction test, two co-ordination tests, a divided attention test, flicker fusion, and proprioception tests were used. The psychomotor skills were measured in the afternoon of the 7th and 14th day of each treatment, 30, 90 and 150 minutes after the second daily administration of the drug in combination with either an alcoholic or a placebo drink. There were no significant differences between the test weeks. Thioridazine alone resembled placebo and had no major combined effect with alcohol. Bromazepam impaired reactive and co-ordinative skills and attention deteriorated. The combination of bromazepam and alcohol potentiated the deterious effects of the single agents, and this effect was most remarkable at 30 minutes. The subjects also gave exaggerated responses in the proprioceptive tests. No significant alterations were recorded in the flicker fusion frequency after any treatment.

Adult↗
PubMed1979

A comparison of clozapine, chlorpromazine, and thioridazine upon DRL performance in the squirrel monkey.

Clozapine (0.16--10 mg/kg, p. o.), chlorpromazine (0.25--2 mg/kg, p. o.), and thioridazine (0.25--2 mg/kg, p. o.) were administered to squirrel monkeys subjected to a DRL 10 s schedule. The reinforcer consisted of 50% unsweetened orange juice. Chlorpromazine and thioridazine had no effect at the lower doses, but decreased response rate at the highest dose. Clozapine increased response rates at the low doses (0.31--2.5 mg/kg) and decreased rates at the high dose (10 mg/kg). Clozapine appears to show a major difference from other neuroleptic drugs in this test by increasing response rate. Since clozapine produces few extrapyramidal side effects in man, this procedure may be useful in selecting and developing new anti-psychotic drugs with less liability for side effects.

Animals↗
PubMed1975

Inhibition of 4,alpha-dimethyl-m-tyramine (H 77/77)-induced hypermotility in rats by single and repeated administration of chloropromazine, haloperidol, clozapine and thioridazine.

The effect of H 77/77 (5 mg/kg s.c.) on motility of rats kept in a familiar cage was investigated. H 77/77 produced hypermotility, which was reduced by oral pretreatment with chlorpromazine, haloperidol, clozapine and thioridazine. The 4 neuroleptics were administered acutely and for a 14 day period. H 77/77 was given 30 min after the single or last dose of neuroleptc (chronic treatment) condition. After both single and repeated administration the neuroleptics showed H 77/77-antagonism in doses ranging from 0.1-2.0 mg/kg. The effect on H 77/77 activity did not change significantly after repeated treatment. Clozapine and thioridazine, which clinically produce only minor extrapyramidal side effects, exert a weak effect or none at all in tests commonly used for neuroleptic activity. These 2 neuroleptics were potent H 77/77-antagonists. Inhibition of H 77/77-hypermotility may possibly be used as a test for neuroleptics.

Adrenergic Agents↗
PubMed1977

Plasma levels and half lives of thioridazine and some of its metabolites. I. High doses in young acute schizophrenics.

Plasma levels of thioridazine and four of its metabolites were determined in a series of fifteen young acute schizophrenics; Consistent individually different metabolic patterns were detected in a group of patients who had the same value for the sum of thioridazine plus metabolites. The apparent volume of distribution and half life were calculated. Clinical evolution tended to correlate best with the level of mesoridazine.

Acute Disease↗
PubMed1979

Neuroleptic, antimuscarinic, and antiadrenergic activity of chlorpromazine, thioridazine, and their metabolites.

Chlorpromazine and thioridazine are widely used antipsychotic agents that are extensively metabolized. Parent compounds and metabolites have diverse pharmacologic activities, and differences in patterns of metabolism may explain differences in therapeutic and side effects from individual to individual. Radioreceptor assays were used to determine the neuroleptic, antimuscarinic, and anti-alpha-noradrenergic potency of chlorpromazine, thioridazine, and their metabolites. The results indicate that these metabolites show a wide range of potencies. The spectrum of activity of a metabolite may be quite different from that of its parent compound. The clinical relevance of these findings to individual differences in drug response is discussed. The combined use of radioreceptor assays and chemical assays in future clinical research is proposed.

Animals↗
PubMed1976

Piperacetazine versus thioridazine in the treatment of organic brain disease: a controlled double-blind study.

In a double-blind cross-over study, 50 geriatric patients with organic brain disease were divided into two groups. One group first received piperacetazine for 15 days and then thioridazine for 15 days. For the other group the sequence was reversed. Piperacetazine proved to be at least as effective as thioridazine and seemed to be more effective against certain target symptoms; side effects were less common and less severe.

Aged↗
PubMed1979

Study of thioridazine cardiotoxic effects by means of His bundle activity recording.

The effect of thioridazine on sinusal automaticity, myocardial excitability and auriculoventricular conduction have been studied in dogs by measuring the spontaneous heart rate, the effective refractory period of the atrial contractile tissue, the time of auriculonodal and infrahisian conduction. Chloralose anaesthetized dogs were administered 10 mg/kg thioridazine hydrochloride via intravenous route. While sinusal automaticity was not altered, conduction times were prolonged in the suprahisian and mainly the infrahisian part and the atrial refractory period increased. These effects are related to quinidine-like properties and consistent with cardiotoxic effects previously reported in clinical practice.

Animals↗