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Results for “Histamine H1 Antagonists”

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At least 19 recordsLinked to original sources
PubMed1987

Histamine H1 receptors on adherent rheumatoid synovial cells in culture: demonstration by radioligand binding and inhibition of histamine-stimulated prostaglandin E production by histamine H1 antagonists.

Histamine H1 receptors have been demonstrated on adherent rheumatoid synovial cells using biochemical and radioligand binding assays in vitro. The addition of histamine (17.8 mumol/l) to nine primary cultures of adherent rheumatoid synovial cells resulted in a two- to 21-fold increase in the production of prostaglandin E (PGE). This increase was inhibited by three H1 receptor antagonists (mepyramine, tripelennamine, and chlorpheniramine) in a dose related manner at concentrations below 10(-6) mol/l. Competitive binding assays with [3H]mepyramine gave ED50 values of approximately 10(-5) mol/l for the three H1 antagonists. H2 receptor antagonists (cimetidine and ranitidine) did not inhibit the histamine induced increase in PGE and did not compete effectively with the binding of H1 antagonists.

Arthritis, Rheumatoid↗
PubMed1998

Histamine-stimulated cytokine secretion from human conjunctival epithelial cells: inhibition by the histamine H1 antagonist emedastine.

The present studies demonstrate that histamine induces the secretion of IL-6, IL-8 and GM-CSF from human conjunctival epithelial cells in a dose- and time-dependent manner. The histamine antagonists emedastine (H1), ranitidine (H2) and thioperamide (H3) were evaluated for their ability to inhibit secretion of these cytokines. Emedastine potently inhibited histamine-induced IL-6, IL-8 and GM-CSF secretion with mean IC50 values of 2.23, 3.42 and 1.50 nM, respectively. Ranitidine and thioperamide failed to inhibit cytokine secretion over a wide dose range. These data suggest that mast cell derived histamine may stimulate inflammatory cytokine production in allergic conjunctivitis via activation of epithelial cell H1 receptors. The histamine H1 antagonist emedastine potently inhibits this response.

Benzimidazoles↗
PubMed1995

Inhibitory effect of terfenadine, a selective H1 histamine antagonist, on alcoholic beverage-induced bronchoconstriction in asthmatic patients.

We wanted to evaluate the effect of terfenadine, a selective H1-receptor antagonist, on alcoholic beverage-induced bronchoconstriction. Eight patients with alcohol-induced asthma received terfenadine (60 mg, twice on the test day) or placebo, with the last dosing 2 h before the test in a double-blind, randomized, cross-over manner. On two separate study days, each subject drank the same brand and volume of alcoholic beverage (beer or Japanese saké), and bronchoconstriction was assessed as change in peak expiratory flow (PEF) over 120 min postchallenge. Inhalation challenges were performed with the same alcoholic beverage with which they had been orally challenged. The mean (SEM) percentage fall in PEF 15, 30, 45, 60, 90 and 120 min after the oral alcohol challenge was significantly reduced from 12.0 (3.1), 17.0 (1.7), 15.8 (2.3), 15.2 (3.4), 16.6 (4.8) and 14.7 (5.2)%, to 2.6 (1.8), 2.1 (1.6), 3.9 (1.2), 5.7 (2.2), 6.5 (2.6), 5.1 (1.6)%, respectively, by terfenadine. No significant bronchoconstriction was observed after the inhalation challenge. We conclude that the release of histamine makes a major contribution to alcoholic beverage-induced bronchoconstriction in Japanese asthmatic patients, and that histamine H1 antagonists may be effective in preventing alcoholic beverage-induced bronchoconstriction.

Adult↗
PubMed2003

[H1 histamine antagonists].

Histamine is an important mediator for early phase allergic reactions that are involved in atopic diseases, mediated by specific IgE antibodies. After allergenic contact, its liberation induces unpleasant symptoms like itching, several manifestations as local vasodilatation, bronchoconstriction, mucus hypersecretion. Antagonists of H1 histamine receptors are the most prescribed drugs, due to their symptomatic effects at the levels of nasal or conjunctival mucosa, and the skin. Their major indications cover allergic rhinitis, either seasonal or perennial, and idiopathic chronic urticaria, as a first line medication. The pharmacological evolution allows to distinguish three generations of products differing at the levels of specificity, long acting period, and toxicity. The authors are discussing the respective benefits of two recent molecules presented as 3rd generation molecules: fexofenadine and levocetirizine, while repositioning their use among available treatment strategy.

Acetates↗
PubMedDate not supplied

[Snake bites in children: antivenom early reaction frequency in patients pretreated with histamine antagonists H1 and H2 and hydrocortisone].

Type and frequency of early reactions (ER) were studied in 24 children aging 2-14 years victims of snake bites who received pretreatment with histamine antagonists H1 (dextrochlorfeniramine) and H2 (cimetidine or ranitidine) and hydrocortisone from 1989 to 1993. None of them had atopy nor received any type of anti-venoms(AV) and antitoxins before. Of 24 children, 15 received bothropic AV (ER in 5), 7 crotalic AV (ER in 5), 1 crotalic plus crotalic-bothropic AV, and 1 elapidic AV (ER in 1). In 3 children severe early reactions were observed and they were classified as severe crotalic accident. Results suggest that pre-treatment did not offer safety protection at the appearance of early reactions.

Adolescent↗
PubMed1986

Some behavioral effects of histamine H1 antagonists in squirrel monkeys.

Graded dose of the histamine H1 antagonists tripelennamine (0.1-3.0 mg/kg), promethazine (0.1-3.0 mg/kg), diphenhydramine (0.3-10.0 mg/kg) and chlorpheniramine (0.3-1.7 mg/kg) increased rates of nonsuppressed responding under a second-order schedule of food presentation to a maximum beyond which responding was increased less or decreased. In contrast, the H2 antagonist, cimetidine, had no effect or decreased responding at the highest doses studied (56.0-100.0 mg/kg). Intermediate doses of tripelennamine, diphenhydramine and promethazine also increased rates of food-maintained responding that were suppressed by electric shock. Maximal increases in rates of suppressed responding were comparable to those produced by effective doses of chlordiazepoxide (3.0-10.0 mg/kg). Under identical conditions, clozapine (0.1-1.0 mg/kg) increased responding to a lesser extent, and d-amphetamine (0.01-0.3 mg/kg) and cimetidine (3.0-100.0 mg/kg) either did not increase or, at the highest doses, only decreased rates of suppressed responding. Doses of tripelennamine and diphenhydramine that increased rates of nonsuppressed and suppressed responding also maintained self-administration in cocaine-trained squirrel monkeys under a second-order schedule of i.v. injection. Rates and patterns of responding maintained by tripelennamine and diphenhydramine were comparable to those maintained by cocaine and d-amphetamine under identical conditions. The results show that histamine H1 antagonists can have pronounced rate-increasing effects on nonsuppressed and suppressed behavior, and that they can serve as reinforcers in monkeys. These effects occur at doses that probably are greater than those required to saturate H1 sites of action in central nervous system and may not be mediated solely through histaminic mechanisms.

Animals↗
PubMed1989

Mechanistic investigation of species-specific thyroid lesions induced by treatment with the histamine H1 antagonist temelastine (SK&F 93944) in rats.

Temelastine (SK&F 93944), an H1 histamine receptor antagonist, induces thyroid histopathological lesions in the rat, indicative of thyroid follicular cell stimulation, at oral doses of 10-33 mg/kg body weight/day. These changes do not occur in the dog or mouse. Endocrinological short-term studies support an increased thyroid follicular activity (increased radioiodide accumulation) with decreased circulating thyroxine (T4) at oral doses at or above 300 mg/kg body weight/day and increased circulating thyroid stimulating hormone (TSH). This is thought to be responsible for the thyroid follicular stimulation following Temelastine treatment. No direct inhibition of thyroid function occurs. Temelastine produces these species-specific changes by enhancing thyroxine clearance from the circulation in the rat, but not in the dog or mouse. In vitro studies with cultured rat hepatocytes suggest that the mechanism behind these changes is a drug-induced increase of hepatocellular T4 binding and uptake which leads to an enhanced metabolic clearance of the hormone.

Animals↗
PubMed1996

Centrally acting histamine H1 antagonists promote the development of amygdala kindling in rats.

We studied the effect of histamine H1 antagonists on the development of amygdala kindling, an experimental model of epilepsy, in rats. The centrally acting histamine H1 antagonists including pyrilamine (mepyramine) and ketotifen showed an acceleration in the rate of electrical stimulation to develop fully kindled convulsive seizures. On the contrary, epinastine, a histamine H1 antagonist which scarcely enters the brain, showed no acceleration. These findings suggest that the central histaminergic neuron system plays an inhibitory role on the seizure development through central histamine H1 receptors.

Amygdala↗
PubMed1998

Infantile spasms associated with a histamine H1 antagonist.

Some anti-allergic agents act as histamine H1 antagonists and induce seizure discharges in epileptic patients. Of these agents, ketotifen has an especially potent effect. We have experienced 2 cases of 4-month-old boys who developed infantile spasms 8 to 10 days after ketotifen administration. They showed almost the same clinical course with regard to their age, the interval between ketotifen administration and the onset of seizures, their symptoms and EEG abnormalities. These cases suggest that the administration of ketotifen to young infants may be hazardous with regard to inducing infantile spasms.

Electroencephalography↗
PubMed1987

Competitive and stereoselective histamine H1 antagonistic effect of cicletanide in guinea-pig isolated ileum.

The histamine H1 antagonistic effects of the racemic form and the enantiomers of cicletanide, a new antihypertensive furopyridine derivative, were investigated in guinea-pig isolated ileum. Both the racemic and the (-) enantiomer behaved as competitive histamine antagonists (pA2 values of 6.8 and 7.2, respectively). The (+) enantiomer was at least 100 times less potent than the (-) enantiomer. The H1-blocking effect of cicletanide is the most potent and is the only stereoselective property so far reported for the drug.

Animals↗
PubMed2004

West syndrome associated with administration of a histamine H1 antagonist, oxatomide.

We report a 4-month-old female infant who developed West syndrome eleven days after administration of a histamine H1 antagonist, oxatomide, for atopic dermatitis. It has been reported that some histamine H1 antagonists induce seizures in epileptic patients. The age, the interval between oxatomide administration, and the onset of West syndrome and its clinical course were similar to two previously reported 3-month-old infants with West syndrome associated with ketotifen administration. We should be cautious in using the histamine H1 antagonists, oxatomide and ketotifen, in young infants because such agents could potentially disturb the anticonvulsive central histaminergic system.

Female↗
PubMed2005

Histamine H1 antagonists block M-currents in dissociated rat cortical neurons.

We investigated the effects of histamine H1 antagonists on acutely dissociated neurons from the rat cortex using the patch-clamp technique. First-generation antihistamines, such as pyrilamine, d-chlorpheniramine, diphenhydramine, and ketotifen, suppressed M-currents in a concentration-dependent manner with respective half-inhibition concentrations (C50) of 35.9, 48.5, 34.8, and 47.8 microM at a holding potential of -26.5 mV. Astemizole, a second-generation antihistamine, inhibited M-currents with a C50 of 18.1 microM, but cetirizine did not do so, up to a concentration of 300 microM. Neither ranitidine nor cimetidine, both H2 antagonists, suppressed M-currents. The C50 of pyrilamine significantly decreased with membrane hyperpolarization, suggesting that it acts directly on M channel pores. The inhibition of M channels may be involved in the neurotoxic effects of histamine H1 antagonist overdose.

Analysis of Variance↗
PubMed1999

Synthesis and structure-activity relationships of 2-(substituted phenyl)-3-[3-(N,N-dimethylamino)propyl]-1,3-thiazolidin-4-ones acting as H1-histamine antagonists.

2-(Substituted-phenyl)-3-[3-(N,N-dimethylamino)propyl]-1,3-thiazolidi n-4- ones (1-15) showed dependence of the potency of the H1-histamine antagonism on the m- and p-substituents suggesting that the aromatic moiety binds the receptor by a strong pi-interaction. Electron-withdrawing substituents decrease the potency while the electron-donating alkyl substituents, enhancing the aryl HOMO energy, increase the antihistamine activity. The m-substituents with the capability to form hydrogen bonds, seems to share an extra-interaction with hydrogen accepting or donating groups of the histamine receptor and exhibits very high potency.

Histamine H1 Antagonists↗
PubMed1995

Histamine H1 receptor occupancy in human brains after single oral doses of histamine H1 antagonists measured by positron emission tomography.

1. Histamine H1 receptor occupancy in the human brain was measured in 20 healthy young men by positron emission tomography (PET) using [11C]-doxepin. 2. (+)-Chlorpheniramine, a selective and classical antihistamine, occupied 76.8 +/- 4.2% of the averaged values of available histamine H1 receptors in the frontal cortex after its administration in a single oral dose of 2 mg. Intravenous administration of 5 mg (+)-chlorpheniramine almost completely abolished the binding of [11C]-doxepin to H1 receptors (H1 receptor occupancy: 98.2 +/- 1.2%). 3. Terfenadine, a nonsedative antihistamine, occupied 17.2 +/- 14.2% of the available H1 receptors in the human frontal cortex after its administration in a single oral dose of 60 mg. 4. There was no correlation between H1 receptor occupancy by terfenadine and the plasma concentration of the active acid metabolite of terfenadine in each subject. 5. PET data on human brain were essentially compatible with those on H1 receptor occupancy in guinea-pig brain determined by in vivo binding techniques, although for the same H1 receptor occupancy the dose was less in human subjects than in guinea-pigs. 6. The PET studies demonstrated the usefulness of measuring H1 receptor occupancy with classical and second-generation antihistamines in human brain to estimate their unwanted side effects such as sedation and drowsiness quantitatively.

Administration, Oral↗
PubMed1991

Histamine(H1) antagonists and airway hyperreactivity in the guinea-pig.

Ketotifen inhibits development of airway hyperreactivity in guinea-pigs exposed to PAF, (+/-)isoprenaline, immune complexes or endotoxin. Ketotifen is not a competitive histamine(H1) antagonist, so that it cannot be concluded that there is mandatory involvement of histamine in the development or expression of these forms of airway hyperreactivity. This conclusion has been reinforced by determining the efficacy of other histamine(H1) antagonists as inhibitors of PAF-induced airway hyperreactivity. When compounds were administered intravenously, at a dosage (1 mg/kg) which fully abolished responses to intravenous histamine, the observed rank order for inhibition of PAF-induced hyperreactivity was: ketotifen greater than cetirizine greater than acrivastine greater than KB-2413 greater than oxatomide greater than azelastine greater than terfenadine = astemizole = clemastine = mepyramine = loratadine = saline. Terfenadine may lack inhibitory activity because of a capacity to induce airway hyperreactivity in the guinea-pig. It can be concluded that inhibition of the development of airway hyperreactivity is not a characteristic of histamine(H1) antagonists.

Airway Resistance↗
PubMed1998

Conditioned place-preference analysis in the goldfish with the H1 histamine antagonist chlorpheniramine.

The aim of this study was to investigate whether the histamine H1-receptor blocker, chlorpheniramine (CPA), has a reinforcing effect in goldfish. We used a place-preference procedure in an aquarium with two chambers colored black and white. On day 1, the animals were placed in the test chamber for 10 min for habituation. On day 2, they were placed in the start compartment for 30 s, the sliding doors were opened, and the time spent in each compartment was recorded over the 10 min to determine the natural compartment preference for each animal. On day 3, they were injected either with 0.1, 0.4, 1.0, or 4.0 mg/kg of CPA or only with vehicle and placed in the less preferred compartment for 25 min. On day 4, the animals were placed in the start compartment and the time spent in each compartment during the 10-min test period was recorded again. The groups treated with 1.0 and 4.0 mg/kg of CPA, spent significantly more time in the compartment in which they experienced the drug effect than the group treated with vehicle. On the other hand, the group treated with 0.4 mg/kg spent significantly less time in the drug-paired compartment. The results indicate a biphasic effect of CPA. Considering that there is evidence that low doses of CPA can also block H3-receptors, we suggest that in goldfish the histaminergic neural system has an inhibitory role in the reinforcing process.

Analysis of Variance↗
PubMed1987

Effect of cetirizine, a new histamine H1 antagonist, on airway dynamics and responsiveness to inhaled histamine in mild asthma.

Cetirizine, a major human metabolite of hydroxyzine, preserves the histamine H1-antagonist activity of the parent compound but poorly penetrates the blood-brain barrier, thus minimizing sedative and anticholinergic effects. In 10 young (mean age 27.7 years) subjects with mild asthma (FEV1 greater than 70% predicted), we evaluated the bronchodilator and protective efficacy of 5, 10, and 20 mg of cetirizine against bronchospasm induced by histamine inhalation (0.03 to 20 mg/ml) in comparison with placebo and hydroxyzine, 25 mg, using a random, double-blind crossover design. The provocative concentration of histamine causing a 20% decline in FEV1 for all 10 subjects from the postdiluent control value was more than fourfold greater after each active drug than after placebo. Cetirizine, 5 to 20 mg, provided significantly greater protection against histamine-induced bronchospasm than hydroxyzine (p less than 0.001); moreover, a dose-dependent protective effect was noted with cetirizine. Significant bronchodilation was also found: at 60 minutes, FEV1 increased significantly after all active antihistamines compared to placebo and after 20 mg of cetirizine compared to hydroxyzine (p less than 0.05). FEV1 increased significantly at 120 minutes after hydroxyzine and after cetirizine in both the 20 and 10 mg doses compared to placebo (p less than 0.05). We conclude that in subjects with mild asthma, orally administered cetirizine provides significant dose-dependent protection against histamine-induced bronchoconstriction, which in the doses studied is superior to that produced by the parent compound, hydroxyzine. In addition, cetirizine in 5 to 20 mg doses causes acute bronchodilation. These results suggest a possible role of cetirizine in asthma therapy.

Administration, Inhalation↗