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PubMed1983

Interaction of neuroleptic drugs with a synthetic calcium-binding peptide analog of site III of rabbit skeletal troponin C. Phenothiazine selective binding.

The effects of nine drugs on the CD spectra of a synthetic calcium binding analog of site III of rabbit skeletal troponin C, can generally be divided into 3 groups: (1) that consisting of haloperidol, benperidol, molindone and promethazine, had no effect on the CD spectrum or calcium sensitivity of the apopeptide; (2) that composed of structurally rigid thioxanthenes, induced CD-detectable structural change in the apopeptide but prevented Ca2+-induced structural change; (3) that consisting of chlorpromazine, trifluoperazine and fluphenazine, induced structural change in the peptide but had no effect on the Ca2+-induced structural change.

Animals↗
PubMed1992

Characterization of Ca(2+)-ATPase of Setaria cervi (Nematoda: Filarioidea): effect of phenothiazines and anthelmintics.

1. A Mg2+ independent, Ca(2+)-ATPase requiring high concentrations of Ca2+ (5 mM) for the activation, equally distributed in cuticle-muscular-hypodermis, genital organs and gastrointestinal tissues and mainly localized in 10,000 g pellet fraction, was identified in Setaria cervi, a bovine filarial parasite. 2. Filarial enzyme showed Km value of 3.33 mM for ATP as computed from the double reciprocal Lineweaver-Burk plot. 3. The enzyme could be completely solubilized by sonication with about 4-fold increase in specific activity of the enzyme. 4. The enzyme showed about 2-fold activation by the calmodulin fractions isolated from S. cervi and rat brain homogenates. 5. The enzyme was highly sensitive to inhibition with some phenothiazine derivatives. Trifluoperazine was observed to be the most potent inhibitor followed by promethazine and chlorpromazine. 6. Some anthelmintics viz. diethycarbamazine and centperazine were found to be highly potent inhibitors of the enzyme, significant inhibition of filarial Ca(2+)-ATPase was also observed with levamisole and suramine. 7. Studies indicate Ca(2+)-ATPase of S. cervi as a potential chemotherapeutic target.

Animals↗
PubMed1995

Enantiomeric separation of basic drugs using N-benzyloxycarbonylglyclyl-L-proline as counter ion in methanol.

Direct separation of enantiomeric amines using mainly N-benzyloxycarbonylglycyl-L-proline (L-ZGP) but also N-benzyloxycarbonylglyclglcyl-L-proline (L-ZGGP) as the chiral counter ion in methanol is described. The solid phase was Hypercarb porous graphitic carbon. Several amines of pharmacological interest (e.g., alprenolol, sotalol, terbutaline, promethazine and trimipramine) were separated with high enantioselectivity (alpha = 1.16-1.98) using L-ZGP and L-ZGGP as chiral selectors. In accordance with ion-pair chromatography, the retention of the enantiomeric amines was found to increase with increasing concentration of the anionic form of L-ZGP. Addition of a base (sodium hydroxide or an alkylamine) in excess of L-ZGP gave rise to a decrease in retention and enantioselectivity. The enantioselective retention was also affected by adding 2-propanol or acetonitrile to the mobile phase.

Chromatography, Liquid↗
PubMed1982

Electrically induced release of radiolabeled histamine from rat hippocampal slices: opposing roles for H1- and H2-receptors.

Rat hippocampal slices were preloaded with 3H-histamine and superfused with physiological medium and electrically stimulated in the absence (S1) and in the presence (S2) of drugs. The electrically evoked 3H-overflow consisted mainly of histamine, was Ca++ dependent and completely blocked by tetrodotoxin, all pointing towards an impulse triggered neuronal release. Mepyramine, promethazine and diphenhydramine the H1-antagonists, inhibited the stimulation evoked histamine release in a dose dependent manner. Burimamide and cimetidine, the H2-antagonists, enhanced the stimulation induced release of histamine whereas dimaprit, the H2-antagonist, had the opposite effect. Histamine by itself did not influence its own release. The observations indicate an opposing role for H1- and H2-receptors in modulating spike induced histamine release and represents a functional consequence of the stimulation of the receptors.

Animals↗
PubMed1985

Analgesic effects of antihistaminics.

The literature provides considerable evidence indicating that several, but not all antihistaminics, are indeed analgesic agents and some are analgesic adjuvants as well. Those for which effectiveness is reported includes diphenhydramine, hydroxyzine, orphenadrine, pyrilamine, phenyltoloxamine, promethazine, methdilazine, and tripelennamine. The proposed mechanisms of analgesic action of antihistaminics are reviewed and discussed. The literature suggests that more than one mechanism of action exists for them. There is considerable evidence suggesting that histaminergic and serotoninergic central pathways are involved in nociception and that antihistaminic drugs can modulate their responses (1). The evidence for a role for norepinephrine and dopamine and the effects of antihistaminics on them are less well established. Still other pathways have been proposed. A greater understanding of pain mechanisms will aid in elucidating the role of antihistaminics in analgesia.

Analgesia↗
PubMed1985

The discriminative stimulus properties of mepyramine.

Rats were trained to discriminate i.p. injections of mepyramine (10.0 mg/kg) from saline. Correct responses on one of the two levers were reinforced with access to a solution of sweetened condensed milk. A level of at least 27 correct responses in the first 30 (90%) was required in consecutive saline and mepyramine training sessions before a test session was conducted. Amongst the antihistamines, mepyramine, tripelennamine and chlorpheniramine all produced dose-related responding on the mepyramine lever, reaching a maximum of over 90% mepyramine-appropriate responses. Both tripelennamine and chlorpheniramine were more potent than the training drug. Diphenhydramine and promethazine produced high levels of mepyramine-appropriate responses, but the 90% level was not reached with any dose tested. The dextrorotatory isomer of chlorpheniramine, which binds with high affinity to H1-receptors, was approximately twice as potent as the racemic mixture. The anticholinergic, scopolamine, and the local anaesthetic, procaine, produced only low levels of mepyramine-appropriate responses. However, 10.0 mg/kg of the anti-depressant imipramine produced over 90% mepyramine-appropriate responses. These results suggest that a discrimination can be formed on the basis of the specific H1-receptor antagonist activity of mepyramine.

Aminopyridines↗
PubMed1986

Possible role of calmodulin in the control of histamine release from human basophil leukocytes.

We investigated the possible role of calmodulin (CaM) in the control of histamine release from human basophil leukocytes using several CaM antagonists. Trifluoperazine (TFP) (10(-6)-2 X 10(-5) M), pimozide (10(-6)-1.5 X 10(-5) M), chlorpromazine (CPZ) (10(-5)-10(-4) M) and promethazine (PMZ) (2 X 10(-5)-10(-4) M) inhibited in vitro histamine secretion from human basophils induced by several immunological (antigen, anti-IgE, and formyl-L-methionyl-L-leucyl-L-phenylalanine: f-met peptide) and nonimmunological (Ca2+ ionophore A23187 and the tumor promoter 12-0-tetradecanoyl-phorbol-13-acetate: TPA) stimuli. Trifluoperazine sulfoxide (TFP-S) and chlorpromazine sulfoxide (CPZ-S), which have very low affinity to CaM, had practically no inhibitory effect on histamine release from human basophils. The inhibitory effect of TFP could be made irreversible by irradiating the cells with UV light. A sulfonamide derivative, the compound N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide hydrochloride (W-7) (2.5 X 10(-5)-2 X 10(-4) M), which selectively binds to CaM, inhibited the release of histamine from basophils. In contrast, the chloride deficient analogue, W-5, which interacts only weakly with CaM, had practically no inhibiting effect. The IC50 for enzyme release by a series of eight CaM antagonists was closely correlated (r = 0.91; p less than 0.001) with the CaM specific binding, supporting the concept that these agents act by binding to CaM and thereby inhibiting histamine release. TFP and W-7 inhibited histamine release in the absence and in the presence of increasing concentrations of extracellular Ca2+. These results emphasize the possible role of CaM in the control of histamine secretion from human basophils.

Basophils↗
PubMed1987

Suncus murinus: a new experimental model in emesis research.

Effects of various emetic and antiemetic drugs were studied using Suncus murinus for its potential use as an experimental model in emetic research. Subcutaneous injection of nicotine bitartrate (10-15 mg/kg), veratrine sulfate (0.5-1.0 mg/kg), emetine dihydrochloride (40-80 mg/kg) and oral administration of copper sulfate (20-100 mg/kg) caused dose-dependent emesis in suncus. The ED50 of nicotine, veratrine, emetine and copper sulfate were 7.9, 0.4, 47.6 and 21.4 mg/kg, respectively. However, subcutaneously injected apomorphine hydrochloride (0.1-100 mg/kg), digitoxin (0.5-1.0 mg/kg) and orally administered emetine dihydrochloride (10-80 mg/kg) did not induce the vomiting. Chlorpromazine and promethazine decreased the emetic effect of nicotine, veratrine and copper sulfate, but scopolamine hydrobromide was not effective. These results indicate that the Suncus murinus is sensitive to various emetic and antiemetic drugs and can be used as a new experimental animal model for the emesis. Emetic behavior of suncus was discussed in comparison with other animals.

Animals↗
PubMed1988

Suncus murinus as a new experimental model for motion sickness.

Characteristics of motion sickness and effects of possible prophylactic drugs were studied using Suncus murinus (house musk shrew) for its potential use as an experimental model in motion sickness. Mild reciprocal shaking (amplitude: 10-40 mm; frequency: 0.5-3.0 Hz) induced vomiting in most of Suncus murinus within 2 min. Adaptation was observed when the motion stimulus was repeated with an interval of 2 to 3 days. During the repetitive motion training, both the ratio of sensitive animals and the number of vomiting episodes decreased, and the time from the start of shaking to the first vomiting was extended. Subcutaneous injection of scopolamine (100 mg/kg), chlorpromazine (8 mg/kg), promethazine (50 mg/kg), diphenhydramine (20 mg/kg), chlorphenylamine (20 mg/kg) and methamphetamine (2 mg/kg) decreased the emetic effect of motion sickness, but pyrilamine (20 mg/kg), meclizine (20 mg/kg) and dimenhydrinate (32 mg/kg) were not effective or very weak. These results indicate that the Suncus murinus is sensitive to the motion stimulus and antiemetic drugs are effective as prophylaxis. The Suncus murinus is useful as a new experimental animal model for motion sickness.

Acceleration↗
PubMed1988

The Paw test: an animal model for neuroleptic drugs which fulfils the criteria for pharmacological isomorphism.

Recently we have developed an animal model which could discriminate between classical and atypical neuroleptic drugs: the PAW TEST. This test measures the ability of rats to spontaneously withdraw its force- and hindlimbs. It was found that the ability of drugs to affect the rat's forelimb retraction time was associated with the liability of the drug to induce so-called extra-pyramidal side-effects in man. Likewise the ability of drugs to affect the rat's hindlimb retraction time was associated with the antipsychotic efficacy of the drug. These data open the perspective that the forelimb retraction time (FRT) is an animal analogue of parkinsonian side-effects, and that the hindlimb retraction time (HRT) is an animal analogue of antipsychotic effects In the present series of experiments we further evaluated the validity of these notions by applying the criteria of "pharmacological isomorphism" as proposed by Matthysse (1). Thus HRT had to fulfil the criteria of pharmacological isomorphism for the therapeutic effects of neuroleptics, whereas FRT had to fulfil these criteria for the parkinsonian side-effects. The results of the present study show that both FRT and HRT met these criteria. Thus both classical and atypical neuroleptics were effective in prolonging HRT, whereas only the classical neuroleptics prolonged FRT (criterion 1); the nonneuroleptic phenothiazine promethazine (as well as the narcotic morphine, the muscle relaxant diazepam and the antidepressant desipramine) were ineffective in this respect (criterion 2); the acetylcholinergic antagonist scopolamine blocked the FRT, but not the HRT (criterion 3); chronic neuroleptic treatment reduced the FRT, but not the HRT (criterion 4). In conclusion the paw test, an animal model for testing antipsychotic drugs, was found to fulfil the criteria for "pharmacological isomorphism". Although the exact mechanism underlying the paw test is as yet unknown, the present data improve its validity as an animal model.

Animals↗
PubMed1975

Evaluation of fetal heart rate in relation to the intrauterine 20 mm Hg level.

The purpose of the author's study was to investigate whether any changes in fetal heart rate (FHR) and in fetal acid-base status could be observed when the intrauterine pressure rises above 20 mm Hg. 16 primigravidae were studied. In 11 out of 16 patients labor was induced by amniotomy, in 9 cases oxytocin was given, and in 12 patients pethidine and promethazine (Phenergan) was administered. Two new parameters were introduced into the study of the collected material: the peak variation in FHR (bpm) i.e. the difference between the highest and lowest FHR over a given period of time; the contraction energy, i.e. the product of duration and intensity of intrauterine contractions as measured from the 20 mm Hg level. In 15 out of 16 women the mean peak variation in FHR was highest during a uterine contraction (greater than 20 mm Hg). After a uterine contraction (less than 20 mm Hg) the mean peak variation did not immediately return to control values. It is suggested that in the 16 patients studied, the increase in FHR peak variation during uterine contraction is basically caused by a slight transient fetal hypoxia, exaggerated during the expulsion period of labor by cord entanglement.

Female↗
PubMed1982

Histidine-induced bizarre behaviour in rats: the possible involvement of central cholinergic system.

Histidine injected intraperitoneally into rats in doses from 400 to 800 mg/kg induced a dose-dependent bizarre behaviour. The behaviour after histidine was similar to that observed after L-DOPA and peripheral decarboxylase inhibition. The bizarre behaviour was antagonized by chloropyramine, ketotifen, clemastine and promethazine, antagonists of histamine H1 receptors, with ED50's of 13.9, 14.2, 21.6 and 22.2 mg/kg, respectively. Cimetidine, an antagonist of histamine H2 receptors, injected intraventricularly at a dose of 100 micrograms, was without effect. The bizarre behaviour after histidine was not changed by antagonists of dopamine, noradrenaline and serotonin receptors, but it was blocked by atropine, indicating involvement of central cholinergic systems.

Animals↗
PubMed1984

Suitability of amfonelic acid-induced locomotor stimulation in mice as a model for the evaluation of classical and atypical antipsychotics.

The potential usefulness of amfonelic acid ( AFA ), a selective dopamine (DA)-releasing agent, in quantitatively assessing the antidopaminergic and antipsychotic potencies of drugs, was evaluated. The procedure consisted of determining the ED50S of a number of neuroleptics in inhibiting the locomotor-stimulant effect of amfonelic acid in mice. These results were compared with the published data on the relative potencies of the neuroleptics to induce catalepsy in rats, to block drug-induced stereotypy and to alleviate psychotic symptoms clinically. It was observed that the amfonelic acid model was as good as, but not superior to, the other three procedures in identifying the potencies of classical antipsychotics. This model, however, was able to predict the clinical effectiveness of two atypical antipsychotics, thioridazine and clozapine, much more accurately than could be achieved by the other methods. Certain other atypical antipsychotics such as, mezilamine , RMI 81, 582, sulpiride and sultopride also produced a dose-related blockade of the amfonelic acid induced locomotor stimulation in mice. The antagonism to amfonelic acid exhibited by mezilamine was weaker, and that of RMI 81,582 was stronger than that of chlorpromazine. Only large doses of the two benzamides were effective in blocking the effect of amfonelic acid, sultopride being about 3 times more effective than sulpiride in this regard. Another analogue of benzamide, YM-09151-2, known to have the profile of a classical antipsychotic, was more effective than haloperidol in blocking the stimulant effect of amfonelic acid. Trebenzomine , which is considered to have the properties of an atypical antipsychotic, although this was proved otherwise when tested clinically, actually potentiated the response of mice to amfonelic acid. Apomorphine antagonized the stimulant effect of amfonelic acid, which could be attributed to its agonist activity at presynaptic DA receptors. Apomorphine has been reported to have clinical antipsychotic effects. Certain non-antipsychotic drugs such as prazosin (but not phenoxybenzamine), promethazine, methysergide, diazepam, as well as the gamm -aminobutyric acid agonists, muscimol and THIP, also inhibited the amfonelic acid-induced locomotor stimulation. In spite of this drawback, the present procedure should prove to be a useful animal model for the evaluation of the antipsychotic potencies of drugs. Its ability to identify the potential usefulness of atypical antipsychotics is noteworthy.

Animals↗
PubMed1987

Presynaptic and postsynaptic effects of histamine and histamine agonists in the superior cervical ganglion of the rat.

Extracellular and intracellular recording techniques were used to study the effects of histamine and the histamine agonists [impromidine (IMP) and 2-thiazolylethylamine (2-TH)] on synaptic transmission in the superior cervical ganglion of the rat in vitro. At the concentrations employed (up to 10(-5) M) these compounds did not produce detectable effects on the electrical properties of the postsynaptic neurons. Histamine produced a dose-dependent reduction in the amplitude of the extracellularly-recorded presynaptic and postsynaptic compound action potential. The H2 receptor agonist impromidine reduced only the postganglionic compound action potential. Cimetidine, a specific H2 receptor antagonist, produced parallel shifts in the log dose-response curves for impromidine. Impromidine also reduced the average size of the evoked excitatory postsynaptic potential. The reduction of the mean amplitude of the excitatory postsynaptic potential was due to a decrease in the amount of acetylcholine (ACh) liberated by each preganglionic volley (mean quantal content, m) and a diminution in quantal size. The H1 receptor agonist, 2-TH produced a dose-dependent increase in the presynaptic and postsynaptic compound action potential and in m. The increase in m was not associated with changes in quantal size. The H1 antagonists, pyrilamine and promethazine, did not prevent facilitation of ganglionic transmission induced by 2-TH. It is concluded that histamine H1 and H2 receptors exist on preganglionic axons, or terminals in sympathetic ganglia of the rat. Activation of H1 receptors facilitates release of ACh whereas H2 receptor activation results in depressed release.

Action Potentials↗
PubMed1991

Involvement of histamine in naloxone-resistant and naloxone-sensitive models of swim stress-induced antinociception in the mouse.

The antinociceptive activity of histamine in male mice has been demonstrated using chemical and thermal noxious stimuli and its involvement in naloxone-sensitive and naloxone-insensitive models of stress-induced antinociception investigated. In the abdominal constriction test, histamine and dimaprit but not histidine, induced antinociception. Compound 48/80 and H1 antagonists (diphenhydramine, mepyramine and promethazine) and large doses of H2 antagonists (cimetidine and zolantidine) produced antinociception in this test. Antinociception induced by histamine was refractory to mepyramine, metiamide and naloxone. Histamine and non-antinociceptive doses of its antagonists had no influence on the naloxone-resistant warm water swim stress-induced antinociception. In the hot-plate test, histamine agonists, except the H3 agonist (R) alpha-methyl histamine (alpha-MeHA), were antinociceptive but all these agents augmented the naloxone-sensitive room temperature swim stress-induced antinociception, after either intraperitoneal or intraventricular injection. The antinociceptive action of dimaprit was not antagonized by zolantidine which, like other histamine antagonists excluding metiamide, also produced antinociception and enhanced room temperature swim stress-induced antinociception. These findings suggest that histamine is involved in pathways mediating antinociception in the mouse and that such pathways are activated in a naloxone-sensitive model of stress-induced antinociception but not in a naloxone-insensitive model.

Animals↗
PubMed1987

The mechanism of acute cytotoxicity of triethylphosphine gold(I) complexes. I. Characterization of triethylphosphine gold chloride-induced biochemical and morphological changes in isolated hepatocytes.

Triethylphosphine gold complexes are effective therapeutic agents used for the treatment of rheumatoid arthritis. Many of those molecules are also highly cytotoxic in vitro and can inhibit DNA and protein synthesis. Preliminary experiments have indicated that triethylphosphine gold chloride (TEPAu) may induce the peroxidative decomposition of cellular membrane lipids. The purpose of these investigations therefore was to evaluate the role of lipid peroxidation in the mechanism of acute cytotoxicity of a gold(I) coordination complex, TEPAu, and to examine the early morphological and biochemical changes induced by TEPAu in suspensions of freshly isolated rat hepatocytes. TEPAu caused a rapid loss of cell viability at concentrations above 25 microM which was significantly different from that of control by 60 min and complete by 180 min of incubation. TEPAu also depleted cells of reduced glutathione (GSH) and increased the formation of malondialdehyde (MDA) by 60 min. Incubation of cells with either of the antioxidants, N,N'-diphenyl-p-phenylenediamine (DPPD) or promethazine blocked the formation of MDA but did not alter the time course of cell death or GSH depletion induced by TEPAu. TEPAu also caused a decrease in cellular NADPH and NADH by 10 min. Electron microscopy of hepatocytes exposed to TEPAu revealed early (5 min) formation of flocculent electron-dense precipitates within condensed mitochondria. These changes characteristically preceded cell death. Energy-dispersive electron-probe microanalysis indicated that the electron-dense precipitates did not contain detectable amounts of gold. TEPAu also caused a concentration-dependent decrease in cellular ATP and oxygen consumption in isolated rat hepatocytes. These data suggest that lipid peroxidation, as indicated by the formation of MDA, is probably not a major mechanism by which triethylphosphine gold complexes lethally injure cells. These data, therefore, suggest that mitochondria may be target organelles in TEPAu-induced toxicity to isolated rat hepatocytes.

Animals↗
PubMed1983

Mechanism of inhibitory effect of some amphiphilic drugs on platelet aggregation induced by collagen, thrombin or arachidonic acid.

The effects of two representative groups of amphiphilic drugs, lysophosphatidylcholine species (myristoyl, palmitoyl and stearoyl) and phenothiazine neuroleptics (promethazine, chlorpromazine and trifluoperazine), on the morphology of intact rabbit platelets, arachidonate release from membrane phospholipids, pseudopod formation and the resulting aggregation of stimulated platelets were examined and compared with those of two known cycloxygenase inhibitors, aspirin and indomethacin. Collagen-induced aggregation was inhibited by relatively low concentrations of amphiphilic drugs in parallel with the prevention of arachidonate release from the membrane phospholipids. Thrombin-and arachidonate-induced aggregations were inhibited by these drugs at higher concentrations, at which they transform intact platelets from discoid to spiny and spherical shape, respectively, and consequently suppress formation of native pseudopods induced by these stimuli. Washing the drug-treated platelets with BSA-Tyrode solution abolished all the effects of drugs. In contrast, the cycloxygenase inhibitors blocked both collagen- and arachidonate-induced aggregations without causing membrane shape change of the intact platelets, although they inhibited thrombin-induced aggregation at extremely high concentrations, at which they did elicit membrane shape change. These observations suggest that these amphiphilic drugs act on the plasma membrane of platelets and impair membrane-linked functions. At lower concentrations they specifically inhibit the arachidonate release from the membrane phospholipids under collagen stimulation; at higher concentrations they drastically perturb the plasma membrane structure, inducing the membrane shape change, and suppressing the native pseudopod formation under thrombin or arachidonate stimulation. The impairment of membrane-linked functions by these amphiphilic drugs is thought to account for their inhibition of stimulus-induced aggregation.

Animals↗
PubMed1987

The thrombopenic effect of ellagic acid in the rat. Another model of platelet stimulation "in vivo".

In the rat, intravenous injection of large doses (30 mg/Kg) of ellagic acid (EA) induced a decrease in the plasma level of fibrinogen and in the blood platelet content and an increase of the activated partial thromboplastin time. The long-lasting thrombocytopenia was inhibited by heparin (4 mg/Kg), defibrase (20 U/Kg), clocoumarol (4 mg/Kg) and CCI 17810 (120 mg/Kg). It was not inhibited by aspirin (90 mg/Kg), indomethacin (8 mg/Kg), ketoprofen (4-10 mg/Kg), epsilon-aminocaproic acid (150 mg/Kg), methysergide (4 mg/Kg), chlorpromazine (10 mg/Kg) and promethazine (4 mg/Kg). On the contrary, the small doses of indomethacin (4 mg/Kg) and of ketoprofen (0.5-2 mg/Kg) increased the thrombopenic effect of EA. EA induced the accumulation of Cr51-labelled platelets into the lungs and the liver, accompanied by a 64% fall in Cr51 blood radioactivity. The platelet stimulating effect of EA would depend on an intravascular coagulation which occurs in the whole cardiovascular system. It is suggested that the pro-aggregating derivatives of arachidonic acid had a minor role in this stimulation. The intravascular coagulation induced by EA was accompanied by a swelling of the lymph nodes and of the spleen. In immune platelet depleted rats, EA induced only the swelling of lymph nodes.

Animals↗