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PubMed1989

Drug interaction of promethazine & other non-conventional antimicrobial chemotherapeutic agents.

The antihistamine compound promethazine (Pz) showed significant antibacterial action when tested against 124 strains of aerobic and 13 strains of anaerobic bacteria belonging to both Gram positive and Gram negative genera. The range of MIC (micrograms/ml) of Pz varied between 50 and 200 micrograms/ml among most of the test organisms. Six Pz-sensitive strains were found to be simultaneously sensitive to similar non-conventional antimicrobics, e.g., methdilazine, bromodiphenhydramine, diphenhydramine, methyl-DOPA, promazine and the antibiotic augmentin. A high degree of synergism was observed in vitro when Pz was used in combination with methdilazine and bromodiphenhydramine.

Anti-Bacterial Agents↗
PubMed1985

[The affinity of aromatic fluoride derivatives of phenothiazine neuroleptics to spiroperidol binding sites of dopamine receptors by the radioligand technic in vitro].

By introduction of fluorine into the position 7 of butaperazine, chlorpromazine, methoxypromazine, perphenazine, prochlorperazine or into the position 3 of promazine derivatives are obtained with higher affinities for the 3H-spiroperidol binding site of the dopamine receptor compared with the corresponding substances free of fluorine.

Animals↗
PubMed1985

[Neuroleptics in psychogeriatrics. A proposal for a more rational prescription policy].

All neuroleptics have a cerebral dopamine receptor blocking effect. This is the best documented explanation for their anti-psychotic effect. Furthermore, they act to a widely differing extent in a blocking manner to other central neurotransmitters, such as noradrenaline, acetylcholine, histamine, and serotonin. During the last couple of years quantitative data have been produced, enabling a more rational choice of neuroleptics. Based on these data and a number of pharmacokinetic considerations, a provisional scheme has been elaborated for the choice of neuroleptics in some clinical situations in psychogeriatrics. Our own experiences with this scheme are promising. It allowed us to restrict the use of neuroleptics to five drugs. The neuroleptics with a strong sedative and anticholinergic action, such as alimemazine, promazine and levomepromazine, being potentially dangerous to particularly elderly patients, are no longer used.

Aged↗
PubMed1988

Antiplasmid activity of tricyclic compounds.

Three representative groups of tricyclic psychopharmacons were shown to have antiplasmid activity. The first group, e.g., comprises promazine, chlorpromazine, promethazine, levo- and dextromepromazine, thioridazine, diethazine, thiethylperazine. There are two heteroatoms (S and N) in the ring system of these compounds. In the second group, which includes desipramine, imipramine, however, there is only one heteroatom N, or S in chlorprothixene, chlorpenthixols and in the third group amitriptyline, maprotiline contain no heteroatoms. The medical significance of plasmid elimination by tricyclic psychopharmacons and related compounds in vitro is that this opens up a new perspective in the struggle against bacterial resistance to antibiotics. This approach utilizes the beneficial side-effect of the plasmid curing ability of these psychopharmacons, and may serve as a guideline for drug design in the future, to develop related substances which are potent in eliminating the drug resistance-carrying plasmids of bacteria, but which have no other pharmacological effects. Here we propose a new mechanism for plasmid curing by tricyclic drugs.

Antidepressive Agents, Tricyclic↗
PubMedDate not supplied

The influence of neuroleptics on the behavioural effect of 5-hydroxytryptophan.

The antagonism of neuroleptics of various groups (chlorpromazine, chlorprothixene, clopenthixol, clozapine, flupenthixol, fluphenazine, haloperidol, levomepromazine, mepazine, perazine, perphenazine, pimozide, prochlorperazine, promazine, spiperone, thiopromazine, thioridazine, trifluperazine, trifluperidol, triflupromazine) towards L-5-hydroxytryptophan (5-HTP) was assessed on the basis of inhibition of characteristic head-twitches. ED50 was assayed in mice and rats. The results indicate that all investigated neuroleptics inhibit the action of 5-HTP and their ED50 values are, as a rule, lower than the values of ED50 for catalepsy. That action is for the majority of neuroleptics more pronounced in mice than in rats. The present paper disucsses possible serotonergic, dopaminergic and also noradrenergic mechanism of action of neuroleptics in the 5-HTP test.

5-Hydroxytryptophan↗
PubMed1987

[Medication and monitoring in young pediatric patients in NMR (nuclear magnetic resonance) studies].

Nuclear magnetic resonance (NMR) is a recently developed, noninvasive technique of increasing importance in pediatric diagnosis. In newborns and very young infants problems may arise with regard to adequate sedation and sufficient patient monitoring during NMR imaging. In 44 of 46 young pediatric patients sedation with oral promazine or rectal diazepam/intravenous ketamine provided good immobilization during NMR scanning. In two patients an additional drug was necessary in order to successfully complete the NMR procedure. Satisfactory monitoring of patients' respiratory motions was obtained by means of a simple optical system. Good cardiovascular monitoring was made possible by lengthening the rubber tubing of a blood pressure cuff. No complications were observed during the NMR-procedures.

Anesthesia↗
PubMed1987

Photoactivation mechanism of hyaluronidase by chlorpromazine.

A pre-irradiated chlorpromazine (CPZ) in pH 7.2 and aqueous solutions activated hyaluronidase, and it showed the enzyme-activating action even after 7 days of irradiation. This indicates that the stable photoproducts of CPZ activated the enzyme. But promazine and CPZ-5-sulfoxide, which are photoproducts of CPZ, did not activate the enzyme in the presence and absence of UVA. The dimer and higher molecular weight (MW) products of CPZ that were obtained by treating the pre-irradiated CPZ solution with gel permeation chromatography showed the hyaluronidase by activating action without UVA. In addition, photoactivation of hyaluronidase by CPZ was inhibited by radical quenchers. This suggested that the photoproducts with enzyme-activating action were produced via some radicals. On the basis of these findings, a possible mechanism for photoactivation of hyaluronidase by CPZ was proposed.

Animals↗
PubMed1979

Elimination of F'lac plasmid by different psychotropic drugs and some related compounds.

Desipramine, trimipramine, protriptyline, noxiptyline, promazine, trimeprazine, triflupromazine and chlorprothixene methoiodide eliminated the F'lac plasmid of Escherichia coli, while thiazinanum, toluidine blue, lidocaine and procaine were ineffective in this respect. The plasmid eliminating action of the drug ceased in the presence of 0.05 M magnesium sulphate. Methylene blue did not inhibit plasmid elimination by the psychotropic drugs, and in presence of the dye even lidocaine and procaine became effective. Based on plasmid elimination in the presence of methylene blue and on the selective effects of the lon- mutant, the plasmid eliminating mechanism of psychotropic drugs seems to differ from that of acridine orange.

Animals↗
PubMed1979

Gas-chromatographic analysis for chlorpromazine and some of its metabolites in human serum, with use of a nitrogen detector.

We describe a gas-chromatographic method for measuring chlorpromazine and its metabolites chlorpromazine sulfoxide, mono-N-desmethylchlorpromazine, and di-N-desmethylchlorpromazine at therapeutic concentrations in human serum, with use of a nitrogen detector. The compounds are extracted from serum at pH 10.5 into hexane/isoamyl alcohol, re-extracted into dilute HCl, and then extracted into hexane after alkalinization of the HCl. The N-desmethylated metabolites are measured as their respective N-trifuloracetyl derivatives; the parent drug and its sulfoxide are measured as the unchanged bases. Promazine is the internal standard. As little as 5 micrograms of chlorpromazine, 20 micrograms of chlorpromazine sulfoxide, 20 micrograms of mono-N-desmethylchlorpromazine, and 10 micrograms of di-N-desmethylchlorpromazine per liter can be measured in 2-mL samples of serum. The within-run coefficients of variation for assays of these drugs at 100 micrograms/L are 2.7%, 5.6%, 5.1%, and 5.3%, respectively. The procedure was applied to patients receiving therapeutic doses of chlorpromazine and to patients who had ingested an overdose of chlorpromazine.

Chlorpromazine↗
PubMed1979

Some properties of 5-hydroxytryptamine receptors in the hindquarters of the rat.

1 The rat hindquarter preparation, as described, responds with reproducible vasoconstriction to noradrenaline and tryptamines. 2 The receptors involved in these responses are distinct. 3 Evidence of heterogeneity of tryptamine receptors was not obtained. 4 The 5-hydroxytryptamine (5-HT) antagonists, methysergide and cyproheptadine, although very potent, displayed antagonism of a non-competitive type whereas a series of phenothiazines and phentolamine displayed competitive antagonism against 5-HT. 5 For the phenothiazines the order of increasing potency was promazine less than chlorpromazine less than triflupromazine.

Animals↗
PubMedDate not supplied

[Effect of neuroleptics, midantan and DOPA on apomorphine sterotypy in rats].

The influence of differently structured neuroleptics on the stereotypyd attitude of rats, induced by apomorphine, was inquired into. Most of the known neuroleptics manifested an inhibitory effect on the apomorphine-induced stereotypy. Clozapine and azabutyrone were effective only in a dose of 25 mg/kg, while carbidine and promazine failed to exert any marked influence on the stereotypy. It seems that the antiapomorphine effect does not correlate with the antipsychotic activity of the neuroleptics.

Amantadine↗
PubMed1977

[Studies on the effect of urapidil on the central nervous system and various organ functions in animal experiments (author's transl)].

Compared to the changes in spontaneous behaviour of mice and rats, 6-(3-[4-(o-methoxyphenyl)-1-piperazinyl]-propyl-amino)-1,3-dimethyluracil (urapidil, Ebrantil) in doses from 10 mg/kg p.o. has a central sedative action, for which it is typical that it can be interrupted by external stimuli after doses of up to approx. 100 mg/kg. By this action urapidil differs from other central-acting drugs, e.g. chlor-promazine, diazepam and clonidine. It can be assumed that urapidil has no central dopamine blocking qualities because it does neither influence the conditioned avoidance response nor the amphetamine-induced gnawing of the rat. Urapidil is also different from diazepam bacause it does not hinder spinal polysynaptic motor reflexes of the decerebrated cat. Up to 80 mg/kg p.o. of urapidil, there was no hypotensive effect in the rat to be seen and, therefore, it can be concluded that changes in spontaneous and reactive behaviour are not due to acute changes in cardiovascular functions. The antihistamine effect of urapidil in the isolated ileum of the guinea pig is approx. 15 times weaker than that of chlorpromazine, furthermore urapidil has no anticholinergic quality.

Animals↗
PubMed1984

Interaction of quaternary phenothiazine salts with calmodulin.

To clarify the role of electrostatic forces in the binding of phenothiazines to calmodulin, the quaternary methiodide salts of several 10-alkylaminophenothiazines were prepared and examined for anticalmodulin activity. In addition, the methiodide salt of [3H]chlorpromazine was prepared and its binding to calmodulin was studied. Both the hydrochloride and methiodide salts of a variety of 10-alkylaminophenothiazines inhibited the calmodulin-induced activation of phosphodiesterase at concentrations that had no effect on the basal activity of the enzyme. The IC50 values for the inhibition of calmodulin by the methiodide salts were similar to those of the corresponding hydrochloride salts, with the compounds displaying the order of potency: trifluopromazine greater than chlorpromazine greater than promazine greater than promethazine greater than chlorpromazine sulfoxide. The acidic compound 3-(2-chloro-10-phenothiazinyl)propionic acid displayed no anticalmodulin activity at concentrations up to 80 microM; at higher concentrations the compound inhibited both basal and calmodulin-stimulated enzyme activity. Other results showed that both chlorpromazine hydrochloride and chlorpromazine methiodide bound to calmodulin in a Ca++-dependent manner. However, the binding of chlorpromazine hydrochloride decreased markedly at alkaline pHs, whereas the binding of chlorpromazine methiodide was not pH-dependent. The fact that the binding of the nondissociable methiodide salt is not pH-dependent, whereas the binding of the hydrochloride salt decreases at pHs at which the drug would be nonionized, indicates that it is the cationic species of the phenothiazine that binds to calmodulin and inhibits its activity.

Animals↗
PubMed1980

Increase of neurotensin content elicited by neuroleptics in nucleus accumbens.

The content of neurotensin immunoreactive material (neurotensin-IR) of nucleus accumbens increases 16 hr after a single injection of 2 mg/kg i.p. of haloperidol; this increase persists for 8 hr or longer. Repeated injections of 2 mg/kg/day of haloperidol i.p. cause a gradual and progressive increase of neurotensin-IR. From 0.32 pmol/mg of protein, it increases to 0.57 pmol/mg (1 week) to 0.62 pmol/mg (2 weeks) and reaches 0.68 pmol/mg (3 weeks). A significant increase of neurotensin-IR content of nucleus accumbens is obtained with 0.5 mg/kg i.p. daily for 2 weeks. Maximal responses are obtained with 1 mg/kg/day in 3 weeks. The striatal neurotensin-IR content of rats injected for 2 weeks with 1 mg/kg/day of haloperidol is also increased. In these rats, the neurotensin-IR content of preoptic area hypothalamus, septum and amygdala failed to increase. The increase of neurotensin-IR material of nucleus accumbens was elicited also by chloropromazine (6 mg/kg), trifluoroperazine (2 mg/kg) and pimozide (1.5 mg/kg) while promazine (10 mg/kg) and promethazine (25 mg/kg) were ineffective. The increase of neurotensin-IR content caused by haloperidol chloropromazine, trifluoroperazine and pimozide in accumbens and striatum suggests a modulation of neurotensin metabolism, synthesis or utilization directly or indirectly through dopaminergic synapses.

Animals↗
PubMed1980

[The neuroleptic efficiency of some butyrophenone and fluorinated phenothiazine derivatives (author's transl)].

The action of butaperazine was diminished and simultaneously prolonged by fluorination in the position 3 or 7 as evidenced by a number of tests (prolongation of the resting time, catalepsy, apomorphine and dexphenmetrazine antagonism, conditioned escape reflex, aggressivity, algesimetry) on the rat and the mouse. The same seems to apply, in principle, to promazine and prochlorperazine. In contrast, the action of 7-fluorperphenazine and its esters with adamantanic acid and decanoic acid was markedly increased, but not prolonged, as demonstrated by a test (conditioned escape reflex) on the rat. The potency of fluphenazine is reached, but not its duration of action. This finding still needs confirmation by other tests. The duration of action of the butyrylphenazine esters was scarcely longer than that of butyrylphenazine. Considerable irritation has been seen at the site of injection. The esters of long-chained fatty acids and fluperidol and trifluperidol seem to be more potent than the parent substances. There is obviously no prolongation of the duration of action. The activity of the haloperidol oxime ethers (and probably of the esters, too) is weak as compared to that of haloperidol. The duration of action is not prolonged.

Animals↗
PubMed1984

Dopamine stimulated glycosylation of brain proteins in vitro is inhibited only partially by dopamine receptor antagonists.

Dopaminergic agonists which act on adenylate cyclase-linked dopamine receptor sites (D1-type) (dopamine, apomorphine and ADTN) induced a dose-dependent increase in the incorporation of L-fucose and D-mannose into glycoproteins of hippocampal, striatal and cortical slices of rat and mouse brain, whilst in rat liver slices dopamine failed to elicit such alterations in protein glycosylation. Testing in slices of rat hippocampus dopaminergic agonists with selective affinity to D2-receptors (bromocriptine, ergometrine) no changes in sugar incorporation into glycoproteins of rat hippocampus were observed. Dopamine stimulated L-fucose incorporation into rat hippocampal glycoproteins was inhibited to a different degree, but almost incompletely by dopamine receptor antagonists like haloperidol, D-butaclamol, promazine and alpha-flupenthixol, whilst chloropromazine and the selective D2-receptor antagonist sulpiride were without any effects. Also serotonin receptor antagonists (cinanserine) and beta-adrenergic receptor blockers (pindolol, alprenolol, practolol) failed to interfere with this dopamine action. But D,L-propranolol enhanced dopamine stimulated glycosylation of rat hippocampal proteins in an additive synergistic manner. This effect appeared to be not related to the antagonistic action of propranolol on beta-adrenergic receptor sites. From our results it is concluded that interactions with dopamine receptor sites (D1-type) is only one part of the mechanism triggering dopamine stimulated glycosylation of brain proteins in vitro.

Adrenergic beta-Antagonists↗
PubMed1981

[Peroral duodeno-jejunal biopsy in children. Indications and personal cases].

In this study we report our experience with 50 intestinal biopsies carried out in 35 children in a 14 months period (October 1979-December 1980) and we also describe the technique we use. The biopsy has been performed by two operators using the Crosby capsule, placed at the duodenojejunal flexure under fluoroscopic screening. For sedation we used oral Promazine and viscous xylocaine and i.v. Metoclopramide and Diazepam; the sedation has been classified in 4 degrees and resulted very good in 40 cases, good in 8 cases and sufficient in 2. The biopsy specimens has been examined with dissecting and light microscope and demonstrated 14 sub-total villous atrophy, 2 severe partial villous atrophy, 5 partial villous atrophy and 29 normal villous morphology. By this technique we made a diagnosis of Coeliac disease in 8 cases, suspected Coeliac disease in 3 cases, Dermatitis Herpetiformis in 3 cases and cow's milk proteins intolerance and post-enteritis syndrome in 1 case. No complications occurred during or after intubation. The AA. confirm the diagnostic value of this investigation, its safety and its very high degree of sensitivity superior to any other test of intestinal absorption.

Adolescent↗
PubMed1978

Uptake, metabolism and efflux of l-alpha-acetylmethadol (LAAM) by rat lung tissue.

The uptake, metabolism and efflux of the longacting narcotic analgesic l-alpha-[2-3H]acetylmethadol ([3H]LAAM) were studied using rat lung tissue slices. Uptake of [3H]LAAM by lung slices incubated in 1 micrometer [3H]LAAM in Krebs-Ringer phosphate buffer was rapid for the first 10 minutes, slow thereafter and reached equilibrium after 30 minutes. Less than 10% of the accumulated radioactivity was found to be in the form of the metabolites noracetylmethadol and methadol. LAAM accumulates in lung tissue primarily by passive diffusion and nonspecific binding. Uptake was against a concentration gradient and could be reduced significantly by iodoacetate or by boiling the tissue and slightly reduced by removing oxygen or Na+ from the medium. However, the uptake process was nonsaturable, was not affected by the removal of Ca++ or glucose from from the medium, lacked stereospecificity and was reversible. Efflux of accumulated [3H]LAAM from lung tissue was a first-order process with an apparent t1/2 of 46 minutes. Many drugs which may possibly be used by patients receiving LAAM, such as methadone, fentanyl, propoxyphene, norpropoxyphene, imipramine, promazine and chlorpromazine, were found to have a significant inhibitory effect on [3H]LAAM uptake and could displace accumulated [3H]LAAM from lung tissue.

Animals↗