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PubMed1995

Analysis of pharmaceutical creams: a useful approach based on solid-phase extraction (SPE) and UV spectrophotometry.

Solid-phase extraction (SPE) using C-18, diol and ion-exchange sorbents followed by UV spectrophotometric (conventional and derivative mode) assay was applied to the analysis of basic, acidic and neutral drugs commercially available in creams. A representative set of drugs (promethazine, chlorhexidine, benzydamine, ketoprofen, ibuprofen, fentiazac, piroxicam, fluorouracil, crotamiton and hydrocortisone acetate) was selected, and for each drug the appropriate SPE conditions (adsorption, washing and elution) were investigated to obtain a practical and reliable sample clean-up. It was shown that the developed SPE procedures were capable of removing interfering cream components (excipients including preservatives) allowing accurate spectrophotometric analyses to be performed. In some applications, derivative spectrophotometry was advantageous over the conventional absorption mode with respect to higher selectivity and versatility.

Pharmaceutical Preparations↗
PubMed1996

Construction and evaluation of PVC conventional and tubular tripelennamine-selective electrodes: their application in pharmaceutical preparations.

The construction and evaluation of tripelennamine conventionally-shaped ion-selective electrodes and tubular detectors for the determination of this compound in pharmaceutical formulations are described. Electrodes with conventional configuration have been constructed without an internal reference solution, using several types of immobilized ionic sensors in PVC. The different electrode membranes were prepared by using tripelennamine tetraphenylborate as ionic-exchanger, dissolved in 2-nitrophenyl octyl ether (type A), dibutylphthalate (type B) and bis-(2-ethylhexyl)sebacate (type C) as plasticizer solvents. The general working characteristics of the different types of conventional electrodes were evaluated in tripelennamine solutions, with adjusted ionic strength, showing a linear response in the concentration range of about 4 x 10(-5) - 1 x 10(-1) M and a slope near the theoretical value. The electrodes presented a fast response (> 20 s) and a high reproducibility (> or = 0.2 mV per day). The electrode selectivity in the presence of some interferents, such as sodium, potassium, lithium, ammonium, chlorpheniramine, diphenydramine, promethazine, meclizine and pentazocine, was good, particularly for those whose sensor membrane was prepared with tripelennamine tetraphenylborate dissolved in 2-nitrophenyl octyl ether (type A). Tubular detectors were also prepared using the same sensor membrane and were evaluated in a low-dispersion flow-injection manifold. Under these conditions the detectors presented response characteristics similar to those of the corresponding conventionally-shaped electrodes. The analysis of different pharmaceutical forms (creams, syrups and gels) gave good results with mean recoveries of 99.8-100.6% when the experiments were conducted by direct potentiometry and 99.9-100.4% where the same determinations were conducted by flow-injection analysis with tubular detectors.

Chemistry, Pharmaceutical↗
PubMed1983

Pre- and postsynaptic effects of dopamine antagonists on dopaminergic synaptic transmission in Helix pomatia.

The rate of transmitter mobilization in identified dopaminergic synapses was decreased by the dopamine antagonists pimozide, chlorpromazine, haloperidol, cis-flupenthixol, curare, clozapine and high concentrations of ergometrine. The depolarizing postsynaptic potential was inhibited by pimozide, chlorpromazine, haloperidol, cis-flupenthixol, curare, clozapine, (+)-butaclamol and high concentrations of ergometrine. The hyperpolarizing synaptic potential was inhibited by naloxone, methysergide, (+)-butaclamol, haloperidol, 6-hydroxydopamine and low concentrations of ergometrine, while pimozide, cis-flupenthixol, trans-flupenthixol, curare, clozapine, promethazine, chlorpromazine and (-)-butaclamol had no clear effect. The presynaptic receptors involved in modulation of the mobilization rate showed similarities with the dopamine receptors mediating depolarizations. The dopamine antagonists changed dynamics of synaptic transmission.

Animals↗
PubMed1994

A retrospective study of risk factors of akathisia in terminally ill patients.

Akathisia is a distressing disorder that manifests as a state of restlessness and motor agitation. We aim to highlight the problem of akathisia to the palliative care physician by identifying and quantifying risk factors in the terminally ill. A retrospective case-control study was utilized to investigate risk factors for akathisia. Medical records of cases (N = 100) and controls (N = 365) archived in a computerized database were downloaded and risk factors determined using conditional logistic regression analyses. Exposure to pharmacologically similar drugs, such as haloperidol [odds ratio (OR), 18.4; 95% confidence interval (CI), 8.2-41.4], prochlorperazine (OR, 8.1; 95% CI, 3.0-21.8), and promethazine (OR, 3.3; 95% CI, 1.3-8.0), conferred an increased risk. Other significant variables were exposure to morphine (OR, 5.3; 95% CI, 1.9-14.2), sodium valproate (OR, 2.5; 95% CI, 1.0-6.4), and sodium bicarbonate/tartrate (Ural) (OR, 4.2; 95% CI, 1.2-15.3). Highlighting factors that predispose patients to akathisia emphasizes that this syndrome should not be forgotten when treating the terminally ill. It is recommended that those drugs identified should be judicially used and carefully monitored.

Adult↗
PubMed1987

Significance of increased secretion of glucocorticoids in mice and rats injected with bacterial endotoxin.

Injection of mice or rats with lipopolysaccharide (LPS) is associated with an increased secretion of glucocorticoids. The high level of mortality following injection of LPS that is noted in adrenalectomized rats can be reversed by dexamethasone or corticosterone. That histamine may be an endogenous mediator of the release of corticosterone caused by LPS is suggested by an attenuation of this corticosterone response by promethazine, an H1 antihistamine. Additional support that LPS-dependent glucocorticoid secretion is mediated, in part, by histamine, is suggested by spleen cell transfer studies revealing differences in the induction of histidine decarboxylase (HDC) synthesis and corticosterone release by the C3H/HeN and C3H/HeJ strains of mice that are differentially sensitive to LPS effects. These and other data on increased levels of histamine and HDC during mitogen-induced lymphocyte blastogenesis, as well as experiments revealing immunomodulatory effects of histamine and histamine agonists and antagonists on lymphocyte blastogenesis, are consistent with the hypothesis that following infection with gram-negative bacteria, the histamine-induced increase in glucocorticoid secretion results in inhibition of HDC in splenocytes, a concomitant attenuation of histamine production, and a resulting return to immune homeostasis.

Animals↗
PubMedDate not supplied

Histamine in brain--its role in regulation of seizure susceptibility.

The influence of drugs affecting the turnover and levels of histamine in brain and histamine antagonists on pentetrazole (PTZ)-induced and electroconvulsive seizure threshold in mice was studied. A 1.5-2-fold rise in histamine brain concentration (induced by treatment with histidine or metoprine), led to a concomitant increase of PTZ-induced seizure threshold. A histidine decarboxylase inhibitor (brocresine) induced a depletion of brain histamine by about 75% for at least 8 h, the seizure threshold was, however, only reduced at 6 and 8 h after the injection. At shorter intervals, the seizure threshold was substantially increased. Treatment with centrally acting H1 antagonists (dimethindene and promethazine) in non-sedative dosage diminished the PTZ seizure threshold significantly; no changes were seen after treatment with H2 and H3 antagonists (oxmetidine, ranitidine, zolantidine or thioperamide) and a H3 agonist (R-alpha-methylhistamine). The electroconvulsive threshold was hardly influenced. It is concluded that histamine has a certain anticonvulsant effect which is mediated through H1 receptors.

Animals↗
PubMed1994

Characteristics of [3H]mepyramine binding in DDT1MF-2 cells: evidence for high affinity binding to a functional histamine H1 receptor.

The binding characteristics of [3H]mepyramine to histamine H1 receptors in the smooth muscle cell line, DDT1MF-2, have been investigated. Competition binding experiments produced dissociation constants (Ki) for mepyramine, (+)-chlorpheniramine, and promethazine of 3.4 nM, 2.6 nM and 0.66 nM, respectively. Saturation binding using [3H]mepyramine produced a Kd of 2.1 nM and a Bmax of 47 fmol/mg protein. These data suggest that a high-affinity [3H]mepyramine binding site can be detected with the characteristics of the "classical" histamine H1 receptor. The low-affinity [3H]mepyramine binding site reported previously [Mitsuhashi, M. and Payan, D.G. (1988) J. Cell. Physiol. 134, 367-375] is predominantly to a secondary [3H]mepyramine site. The "low affinity" or secondary [3H]mepyramine binding site on DDT1MF-2 cells is insensitive to quinine (10 microM) and is therefore distinct from the [3H]mepyramine binding protein found in rat liver.

Animals↗
PubMed1994

Inhibition by histamine H1 receptor antagonists of endogenous glibenclamide-sensitive K+ channels in follicle-enclosed Xenopus oocytes.

Effects of histamine receptor ligands on the glibenclamide-sensitive K+ currents induced by K+ channel openers, cromakalim and Y-26763, were examined in follicle-enclosed Xenopus oocytes. Histamine H1 receptor antagonists, promethazine, dimethindene and chlorpheniramine all decreased cromakalim-induced K+ currents with IC50 values of 31.5 microM, 29.5 microM and 138 microM, respectively. These compounds also blocked Y-26763-induced K+ currents with comparable IC50 values. Histamine (1 mM) and histamine H2 receptor antagonists, cimetidine (0.5 mM) and ranitidine (1 mM) had little effect on these K+ currents. These results suggest that histamine H1 receptor antagonists inhibit glibenclamide-sensitive K+ currents by a mechanism other than the histamine H1 receptor antagonism. The inhibitory effects might explain, in part, the reported actions of histamine H1 receptor antagonists in ischemia.

Animals↗
PubMed1991

A three-year photopatch study in Thailand.

Photopatch testing was performed on 274 patients who had history of photosensitivity at the Institute of Dermatology Thailand from 1987 through 1989. A total of 92 positive photocontact reactions and 71 positive contact reactions were seen. The most frequent positive photopatch test reactions were to sulfanilamide (18.2%) followed by Jadit (4.4%) chlorpromazine (3.6%) promethazine (3.6%) and fenticlor (3.2%). The most common photodermatoses was polymorphous light eruption (60.9%). Photocontact dermatitis was established in 28 patients (10.2%) while other skin diseases aggravated by sunlight were seen in 47 patients (17.2%).

4-Aminobenzoic Acid↗
PubMed1991

m-trifluoromethylphenylpiperazine and m-chlorophenylpiperazine-induced hypothermia in mice is reversed by tricyclic antidepressants and other drugs.

Many antidepressants reverse arylpiperazine-induced hypothermia after acute treatment by a mechanism that does not seem to implicate monoamine uptake inhibition. Activity is found in reversing 1-(m-trifluoromethylphenyl)piperazine (TFMPP)-induced hypothermia by desipiramine 5 and 10 mg/kg and not by maprotiline 10 and 20 mg/kg. Clomipramine and fluoxetine with comparable serotonin uptake blocking potential do not have comparable TFMPP-reversing effects. A dibenzothiadiazepine compound (IM/P/3/4), hypothesized to have antidepressant activity though devoid of uptake blocking properties, was active at 10 and 20 mg/kg. Other classes of tricyclics such as neuroleptics (clozapine 5 and 10 mg/kg) and chlorpromazine (2 and 10 mg/kg) and the H1 antihistamines, promethazine (20 mg/kg) and cyproheptadine (10 mg/kg) are active, as well as the calcium antagonists nifedipine (10 mg/kg) and verapamil (10 mg/kg). We hypothesize that properties other than monoamine-uptake block which these compounds share (such as calcium-uptake inhibition) could be involved. Activity was also seen with the 5-HT1A agonists 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT, at 0.05 and 0.25 mg/kg), and 5-methoxy-N,N-dimethyltryptamine (5-MeODMT at 3 mg/kg) as well as with the muscarinic agonist oxotremorine (0.1 mg/kg).

Animals↗
PubMed2003

Emetic action of the prostanoid TP receptor agonist, U46619, in Suncus murinus (house musk shrew).

The emetic action of the prostanoid TP receptor agonist, 11alpha,9alpha-epoxymethano-15S-hydroxyprosta-5Z,13E-dienoic acid (U46619; 300 microg/kg, i.p.), was investigated in Suncus murinus. The emetic response was reduced by 76% following bilateral abdominal vagotomy (P<0.001) and by reserpine (5 mg/kg, i.p., 24 h pretreatment; P<0.05) but U46619 administered i.c.v. (30-300 ng) was not emetic, suggesting a peripheral mechanism involving monoamines. However, fenfluramine (5 mg/kg, repeated treatment) and para-chlorophenylalanine (100-400 mg/kg) and ondansetron (0.3-3 mg/kg) were inactive (P>0.05) to reduce U46619-induced emesis precluding a role of 5-HT and 5-HT(3) receptors in the mechanism. Similarly, phentolamine (0.3-3 mg/kg), propranolol (3 mg/kg), and their combination, and metoclopramide (0.3-3 mg/kg), domperidone (0.3-3 mg/kg), droperidol (0.3-3 mg/kg), scopolamine (0.3-3 mg/kg) and promethazine (0.3-3 mg/kg) were inactive (P>0.05) to reduce the retching and vomiting response. However, the tachykinin NK(1) receptor antagonist, (+)-2S,3S(-3-(2-methoxy-5-trifluoromethoxybenzyl)amino-2-phenylpiperidine) (CP-122,721; 1-10 mg/kg) antagonized emesis (P<0.01). In conclusion, U46619-induced emesis appears to be mediated via a predominant peripheral mechanism sensitive to reserpine and is not likely to involve adrenoceptors, dopamine, 5-HT(3), muscarinic or histamine (H(1)) receptors. The action of CP-122,721 to reduce U46619-induced emesis extends the spectrum of anti-emetic action tachykinin NK(1) receptor antagonists to mechanisms involving TP receptors.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2006

Differential action of anti-emetic drugs on defecation and emesis induced by prostaglandin E2 in the ferret.

In the present studies we investigated the mechanism of action of prostaglandin E2 (1 mg/kg, i.p.) to induce emesis and defecation and/or tenesmus in the ferret. The emesis was antagonized significantly (P<0.05) by ondansetron (0.3 and 1 mg/kg, i.p.) and (+)-(2S,3S)-3-(2-methoxybenzylamino)-2-phenlypiperidine hydrochloride (CP-99,994; 10 mg/kg, i.p.), but neither compound reduced defecations and/or tenesmus, with ondansetron (0.3 mg/kg) actually producing a slight increase (P<0.05). Droperidol (1 and 3 mg/kg), metoclopramide (0.3 and 3 mg/kg), domperidone (0.3 and 3 mg/kg), promethazine (0.3 and 3 mg/kg) and scopolamine (0.3 and 3 mg/kg) failed to reduce prostaglandin E2 induced emesis. However, droperidol (1 and 3 mg/kg) and scopolamine (0.3 and 3 mg/kg) reduced significantly the defecatory and/or tenesmus response (P<0.05). Bilateral abdominal vagotomy was ineffective to reduce emesis and defecations and/or tenesmus. The data suggests that 5-HT3 receptor and NK1 tachykinin receptor antagonists could be useful in the clinic to prevent emesis but not defecations induced by prostaglandin E2.

Animals↗
PubMed2006

A method for screening for various sedative-hypnotics in serum by liquid chromatography/single quadrupole mass spectrometry.

A screening method for the detection of sedative-hypnotics in serum is described. The target drugs, which include practically all the sedative-hypnotics distributed in Japan, consisted of 5 barbiturates, 30 benzodiazepine-related drugs and 11 other sedative-hypnotics (i.e., apronalide, bromisovalum, chloral hydrate, triclofos, chlorpromazine, promethazine, diphenhydramine, hydroxyzine, zopiclone, zolpidem and tandospirone). Thirty-nine analytes, selected in terms of the pharmacokinetics of the target drugs, in human serum were screened using a combination of mixed-mode solid-phase extraction and liquid chromatography/electrospray-ionization single-quadrupole mass spectrometry. The detection limits (non-basic analytes, 1-50 ng/ml; basic analytes, 0.1-5 ng/ml) were sufficient to permit the screening of a single therapeutic administration of a target drug.

Female↗
PubMed2006

Evaluation of drug utilization and prescribing errors in infants: a primary care prescription-based study.

The purpose of this study is to evaluate the drug utilization trends and to describe the prevalence and type of medication-related prescribing errors in infants treated at primary care health centers in Bahrain. Prescriptions issued for infants were collected over a 2-week period in May 2004 from 20 health centers. Prescribing errors were classified as omission (minor and major), commission (incorrect information) and integration errors. Medications were classified according to the British National Formulary. In infants with a mean age of 6.5 months (+/-3.1) drugs per prescription were 2.52 (+/-1.1). Paracetamol and sodium chloride nasal drops were the topmost prescribed systemic and topical drugs, respectively. In 2282 prescriptions, 2066 (90.5%) were with omission (major), commission, and integration errors. In 54.1% of prescriptions with omission errors, length of therapy was not specified in 27.7%, and in 12.8% the dosage form was not stated. In 43.5% of prescriptions with errors of commission, dosing frequency (20.8%) and dose/strength (17.7%)-related errors were most common. Errors of integration such as potential drug-drug interaction comprised 2.4% of all prescribing errors. The proportion of drugs prescribed irrationally were: contraindicated medications, notably chlorpheniramine, promethazine, and corticosteroids (16.1%); medications prescribed on a p.r.n. basis (13.3%); missed information regarding strength of medications (2.8%); medications prescribed over extended periods (2.7%); low dosing frequency (2.6%); supratherapeutic doses (2.3%); excessive dosing frequency (0.8%). Irrational drug therapy in infants, with prescribing errors were apparent in primary care practice, which may be related to a lack of drug information, pharmacovigilance programme, and nonadherence to basic principles of prescribing. Establishing a national drug policy and pharmacovigilance programme for promoting rational drug use are to be considered. There is also a need to evaluate the effectiveness of interventions by measuring the outcomes.

Bahrain↗
PubMed2006

The hypotensive mechanisms for the aqueous stem bark extract of Musanga cecropioides in Sprague-Dawley rats.

The present study was designed to evaluate the hypotensive properties and the mechanisms of action of the stem bark aqueous extract of Musanga cecropioides R.Br. Apud Tedlie (MCW) in anesthetized rats of Sprague-Dawley strain, through an invasive direct blood pressure measuring procedure. Thirty adult rats, weighing 150-230 g, were grouped into five groups of six rats each. The effects of the intravenous graded doses (0.0005-0.05 mg/kg) of the extract on the blood pressure indices were investigated. Its underlying mechanisms were also studied using additional five groups of rats. The results showed that the extract caused a dose dependent fall in the systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure and heart rate of the rats. Bilateral carotid artery occlusion (BCO) caused a reflex increase in mean arterial pressure and heart rate which were significantly attenuated by the extract injection. Angiotensin Converting Enzyme (ACE) blockade with 5 mg/kg of Captopril and cholinergic blockade with 0.2 mg/kg of atropine significantly attenuated the hypotensive response to MCW. However, the pattern of MAP fall in rats pretreated with a combination of Promethazine (1 mg/kg) and Cimetidine (15 mg/kg) was not significant. The results of the study was able to demonstrate dose dependent hypotensive effect of MCW and that its vasorelaxant effects may be through inhibition of sympathetic, cholinergic control of the arterial pressure and most significantly through ACE blockade. However, the phytochemical, elemental and toxicological studies of this potential antihypertensive still needed to be investigated.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2005

Analysis of pharmaceutical preparations containing antihistamine drugs by micellar liquid chromatography.

Rapid chromatographic procedures for analytical quality control of pharmaceutical preparations containing antihistamine drugs, alone or together with other kind of compounds are proposed. The method uses C18 stationary phases and micellar mobile phases of cetyltrimethylammonium bromide (CTAB) with either 1-propanol or 1-butanol as organic modifier. The proposed procedures allow the determination of the antihistamines: brompheniramine, chlorcyclizine, chlorpheniramine, diphenhydramine, doxylamine, flunarizine, hydroxyzine, promethazine, terfenadine, tripelennamine and triprolidine, in addition to caffeine, dextromethorphan, guaifenesin, paracetamol and pyridoxine in different pharmaceutical presentations (tablets, capsules, suppositories, syrups and ointments). The methods require minimum handling sample and are rapid (between 3 and 12 min at 1 mLmin(-1) flow rate) and reproducible (R.S.D. values<5%). Limits of detection are lower than 1 microgmL(-1) and the recoveries of the analytes in the pharmaceutical preparations are in the range 100+/-10%.

1-Butanol↗
PubMed2005

Evaluation of phototoxic and photoallergic potentials of 13 compounds by different in vitro and in vivo methods.

Phototoxic side effects of pharmaceutical and cosmetic products are of increasing concern for patients, dermatologists and the chemical industry. Moreover, the need of new chemicals and drugs puts pressure on pre-clinical test methods for side effects, especially interactive adverse-effects with UV-light. So, the predictive potential of different established test methods, which are used regularly in our departments in order to detect the phototoxic potential of chemicals, were analyzed. Namely the fibroblast 3T3 test, the photo hen's egg test, a guinea pig test for measuring acute photoreactions, and a modified Local Lymph Node Assay, the Integrated Model for the Differentiation of Skin Reactions. Various agents with different photoreactive potential were tested: quinolones like Bay y 3118, ciprofloxacin, enoxacin, lomefloxacin, moxifloxacin, ofloxacin, sparfloxacin, as well as promethazine, chlorpromazine, 8-methoxypsoralen and olaquindox serving as control. Special emphasis was taken to evaluate the capability of the employed test procedures to predict phototoxic side effects in patients. Following our results, both in vitro assays were useful tools to detect photoirritancy while the photoallergic potentials of tested compounds were exclusively detected by an in vivo assay. As long as no in vitro model for photoallergy is available, the UV-IMDS should be considered to evaluate photoallergic properties of a supposed photoreactive agent.

Animals↗
PubMed2005

Motion sickness is linked to nystagmus-related trigeminal brain stem input: a new hypothesis.

Motion sickness is a common and distressing but poorly understood syndrome associated with nausea/vomiting and autonomic nervous system accompaniments that develops in the air or space as well as on sea or land. A bidirectional aetiologic link prevails between migraine and motion-sickness. Motion sickness provokes jerk nystagmus induced by both optokinetic and vestibular stimulation. Fixation of gaze or closure of eyes generally prevents motion sickness while vestibular otolithic function is eliminated in microgravity of space, indicating a predominant pathogenetic role for visuo-sensory input. Scopolamine, dimenhydrinate, and promethazine reduce motion-related nystagmus. Contraction of extraocular muscles generates proprioceptive neural traffic and can provoke an ocular hypertensive response. It is proposed that repetitive contractions of the extraocular muscles during motion-related jerk nystagmus rapidly augment brain stem afferent input by increasing proprioceptive neural traffic through connections of the oculomotor nerves with the ophthalmic nerve in the lateral wall of the cavernous sinus as well as by raising the intraocular pressure thereby stimulating anterior segment ocular trigeminal nerve fibers. This verifiable hypothesis defines the pathophysiological basis of individual susceptibility to motion sickness, elucidates the preventive mechanism of gaze fixation or ocular closure, advances the aetiologic link between MS and migraine, rationalizes the mechanism of known preventive drugs, and explores new therapeutic possibilities.

Afferent Pathways↗