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At least 973 records · Page 54Linked to original sources
PubMed1983

[Effect of antihistaminic preparations on gastric secretion in rats].

Experiments were made to study the influence of a new antihistaminic drug phencarol [(quinuclidyl-3) diphenylcarbinol hydrochloride] on gastric secretion in rats. Unlike the blockers of H1-histamine receptors (diphenhydramine, omeril, pyrilamine, and cyproheptadine), phencarol reduces secretion and the content of free hydrochloric acid in the gastric contents. The antacid activity of the drug is similar to that of the H2-receptor blocker, cimetidine. However, phencarol differs from the latter drug in the mechanism of action. The antacid action of phencarol is likely to be the result of its activation effect on diamine oxidase, which leads to a decrease in the content of active histamine in the tissues and diminution of its supply to H2-histamine receptors that control gastric secretion.

Animals↗
PubMed1980

Controlled comparison of anew antihistamine-decongestant combination to its individual components.

A new antihistamine-decongestant combination tablet, containing azatadine maleate and pseudoephedrine sulfate, was compared to its individual ingredients and also to placebo, in a double-blind, randomized parallel-group clinical study. Two patient groups were treated, one with seasonal allergic rhinitis for two days during the peak of the ragweed season, and another with perennial allergic rhinitis for an extended six-week period. In both groups the combination was found better than its single components, and all three treatments better than placebo, in relieving the symptoms of allergic rhinitis. A few patients reported a transient drowsiness attributable to azatadine.

Cyproheptadine↗
PubMed1984

[Antihistaminic therapy of chronic urticaria. Results of a multicenter study with azatadine and terfenadine].

A comparative double-blind multicenter trial was carried out in six German dermatology clinics involving patients with long-term continuous urticaria. After a five-day washout and initial assessment of the urticaria symptomatology oral antihistamine treatment was started with 2 X 1 mg Azatadine or 2 X 60 mg Terfenadine daily. After seven to ten days' treatment the target symptoms wheals, erythema and itching recovered in all but 4% of the azatadine patients and 21% of the terfenadine patients. Azatadine showed significantly stronger antiallergic efficacy for all symptoms. Both substances caused a certain degree of sedation, but in varying intensity. In all patients developing sedation this undesired side effect disappeared after three days in spite of continuous therapy.

Adult↗
PubMed1984

A specific antihistaminic premedication anti H1 anti H2 for pediatric anesthesia.

The danger of the anaphylactoid reactions which occur during pediatric general anesthesia leads the authors to use a specific antihistaminic premedication. The association of cimetidine and hydroxizine has been proved to be adequate to avoid systemic histamine adverse effects and to diminish gastric secretion in pediatric anesthesia. The authors recommend oral administration.

Anaphylaxis↗
PubMed1993

Antiallergic profile of the novel H1-antihistaminic compound levocabastine.

Levocabastine hydrochloride (R50 547, CAS79516-68-0) caused no inhibitory effect on the histamine release from rat peritoneal mast cells induced by compound 48/80, A23187 and concanavalin A. However, the drug inhibited histamine release from passively sensitized mast cells and passive peritoneal anaphylaxis in rats, though higher concentrations or doses were required. Moreover, levocabastine provided a relatively potent inhibitory effect on histamine release from lung pieces of actively sensitized guinea pigs exposed to antigen, and simultaneously the drug prevented a decrease in the cyclic AMP (cAMP) content. Levocabastine potently inhibited histamine-induced cutaneous reactions in rats and the drug also prevented histamine-induced contraction of isolated guinea pig ileum. Levocabastine did not induce any significant changes in platelet aggregation or in the contraction of guinea pig ileum induced by platelet activating factor (PAF). However, the drug inhibited eosinophil migration induced by PAF. The chemotaxis of neutrophils induced by N-formyl-methionyl-leucylphenylalanine (fMLP) was also inhibited by levocabastine in a dose-dependent fashion. Levocabastine has no influence on the order parameter tested with liposomes, suggesting that the drug provides no significant effect on the membrane fluidity of lipid bilayer. These results seem to indicate that the antiallergic effect of levocabastine is mainly dependent on its potent antihistaminic activity.

Anaphylaxis↗
PubMed1995

Blockade of multiple human cardiac potassium currents by the antihistamine terfenadine: possible mechanism for terfenadine-associated cardiotoxicity.

Use of the antihistamine terfenadine has been associated with QT prolongation and torsade de pointes. One possible mechanism is blockade of cardiac potassium channels. We therefore characterized the effects of terfenadine on potassium currents recorded from isolated human cardiac myocytes. We demonstrated terfenadine block of the transient outward current and a novel, ultra-rapidly activating, delayed rectifier K+ current (IKur), which is very sensitive to 4-aminopyridine. IKur is probably produced by the protein product of Kv1.5a, a Shaker-like potassium channel cDNA cloned from human heart. We also compared terfenadine blockade of fHK (Kv1.5a) currents stably expressed in a human embryonic kidney cell line with terfenadine blockade of IKur in human atrial myocytes. Using the patch-clamp technique, we found that terfenadine produced a time-dependent reduction in Kv1.5a current that was consistent with blockade from the cytoplasmic side of the channel. The terfenadine-sensitive Kv1.5a current in human embryonic kidney cells was similar to the 4-aminopyridine-sensitive current in human atrial myocytes. In addition to blockade of the transient outward current and IKur, terfenadine at clinically relevant concentrations blocked both the rapidly and slowly activating components of the delayed rectifier in human atrial myocytes. Blockade of these K+ currents may contribute to the cardiotoxicity associated with terfenadine usage.

Atrial Function↗
PubMed1993

Non sedating antihistamines.

The development of the newer, non sedating antihistamines represents a real advance in the management of the allergic patient. More recently, rare reports of serious adverse events with two of these agents have been published. Providing the warnings and recommendations are adhered to, these drugs remain effective and safe agents.

Astemizole↗
PubMedDate not supplied

Oxidation of the antihistaminic drug terfenadine in human liver microsomes. Role of cytochrome P-450 3A(4) in N-dealkylation and C-hydroxylation.

The antihistaminic drug terfenadine, alpha-[4-(1,1-dimethylethyl)phenyl]-4-(hydroxydiphenylmethyl)-1- piperidinebutanol (Seldane), is of interest because of its lack of sedative properties. Major routes of metabolism include oxidative N-dealkylation to 4-(hydroxydiphenylmethyl)-piperidine (1) and oxidation of a tert-butyl methyl group to a primary alcohol (2), which is subsequently oxidized to a carboxylic acid. Rates of formation of 1 and 2 varied approximately 30-fold in the 17 human liver microsomal samples examined and were highly correlated with each other, suggesting that the same enzyme may be involved in both oxidations. The rates of formation of 1 and 2 were both correlated with rates of nifedipine oxidation (a marker of cytochrome P-450 (P-450) 3A4) but not with markers for other human P-450s. Microsomal oxidation of (both enantiomers of) terfenadine to 1 and 2 was markedly inhibited by gestodene, a selective mechanism-based inactivator of P-450 3A enzymes but not by any of several other P-450 inhibitors. Antibodies raised against P-450 3A4 could inhibit most of the oxidation of (both enantiomers of) terfenadine to 1 and 2 in a microsomal sample having high catalytic activity but antibodies recognizing other P-450s had no effect. The oxidation of terfenadine to 1 and 2 was catalyzed by purified human liver microsomal P-450 3A4 and by partially purified yeast recombinant P-450 3A4. These results provide evidence that P-450 3A4 (and possibly other P-450 3A enzymes) play a major role in the oxidation of (both enantiomers of) terfenadine to both of its major oxidation products.(ABSTRACT TRUNCATED AT 250 WORDS)

Contraceptives, Oral↗
PubMedDate not supplied

[The effects of benzodiazepine drugs and antihistamines in experimental postinfarct arrhythmias].

Death as consequence of myocardial infarct is most frequently produced by ventricular arrhythmias. The purpose was to study if some antihistamines and benzodiazepines could reduce the incidence of these arrhythmias in the experimental myocardial infarct of the dog. The anterior descending left coronary artery was dissected and tied it twofold. Ten dogs received 150 ml of isotonic saline solution (i.v.) one hour before the occlusion, this was the control group. We integrated five more experimental groups, each one received, before the ligation, one of the following drugs (i.v.): lidocaine (2 mg/kg, n = 16), clonazepam (20 mcg/kg, n = 16), flunitrazepam (30 mcg/kg, n = 25), terfenadine (2 mg/kg, n = 11) and astemizol (1 mg/kg, n = 16). Control recordings of cardiac frequency, blood pressure and ECG were made 10 minutes before occlusion and every 5 minutes for 90 minutes after the occlusion was performed. Prevention of the presentation of ventricular fibrillation for each group was: Control 20%, lidocaine 81.24%, clonazepam 50%, flunitrazepam 76%, terfenadine 54.6%, and astemizol 75%. From this results we concluded that lidocaine, flunitrazepam and astemizol have the largest activity to prevent ventricular arrhythmias in the experimental myocardial infarct of dogs.

Animals↗
PubMed1978

[Inhibition of non-cytotoxic histamine liberation from isolated rat mast cells by antihistaminic preparations].

Phenothiazines (chlorpromazine and promethazine) and antihistaminic quinuclidine derivatives [phencarol, quinuclidyl-3-di-(o-tolyl) carbinol, hydrochloride quinuclidyl-3-di-(o-methoxyphenyl) carbinol--HQMC] at concentrations preceding the histamine-releasing ones inhibited the compound 48/80-induced histamine release from the isolated rat mast cells. HQMC inhibited histamine release induced by selective liberators (compound 48/80, MCD-peptide, specific antigen), but potentiated histamine release induced by nonselective liberators (chlorpromazine, tryton X-100). The inhibition by HQMC of histamine release induced by compound 48/80 increased during 1 min and was reversible. The inhibitory effect of all the compounds tested was partially counteracted by glucose.

Animals↗
PubMed1993

Seasonal allergic rhinitis and antihistamine effects on children's learning.

Children suffering from seasonal allergic rhinitis and matched normals were instructed on the use of a didactic computer simulation in a realistic classroom situation. Groups of atopic children received different treatments before instruction; ie, sedating (diphenylhydramine HCl) or nonsedating (loratadine) antihistamines or placebo. All returned after 2 weeks for an examination measuring factual and conceptual knowledge and the application of a learned strategy. Examination results showed large and consistent impairing effects of the allergic reaction on prior learning. Both the placebo and diphenhydramine groups learned significantly less than normal controls. The loratadine group's learning performance was superior to either of the other atopic groups' but still inferior to the normals'. Our conclusions are that the allergic reaction reduces learning ability in children and that this effect is partially counteracted by treatment with loratadine and aggravated by diphenhydramine.

Child↗
PubMedDate not supplied

H1-antihistamines and prescription compliance.

H1-antihistamines (H1A) have been used for more than 50 years in the treatment of allergic pathology. Their widespread consumption and the growing pharmaceutical offer is noteworthy. Despite this, we have not found any study on the compliance of these drugs in the scientific literature reviewed. The aims of this study are to evaluate compliance with the prescription of H1A in a sample of allergic patients diagnosed as pollen rhinoconjunctivitis (PRC), and to evaluate the possible association between the degree of compliance and certain patient-dependent parameters (age, sex, cultural level, knowledge of the prescription and treatment [duration, number of drugs, posology, method of administration and appearance of adverse drug reactions]). The sample size was 300, and 164 were attended. Of these 164 patients, 123 claimed to have taken correctly the H1A prescribed by the allergologist. Of the group of patient claiming to have followed treatment correctly, only 8 patients did not remember the number of packs of H1A bought, nor their price, nor the appearance of the tablets (or solution). Regarding the frequency of use, 101 patients took the H1A daily, and the remaining 22, depending on symptoms. Administration of the H1A was always oral-tablets in 114 cases and solution in 9. The compliance we have found is at a medium level, similar to that reported in other studies (although on other drugs), and no significant differences were found in relation to the parameters studied.

Adolescent↗
PubMed1995

Individual differences in central nervous system response to antihistamines (H1-receptor antagonists).

HYPOTHESIS: We hypothesized that the objectively documented central nervous system response to antihistamines (H1-receptor antagonists) could not be predicted reliably by an individual's subjective perception of somnolence after ingestion of these medications. METHODS: In a double-blind, placebo-controlled, single-dose, four-way crossover study, cetirizine 10 mg, hydroxyzine 50 mg, diphenhydramine 50 mg, or placebo were administered to 20 healthy subjects. Before and two to two and one-half hours after dosing, the latency of the P300 event-related potential (P300) at the central (Cz) and parietal (Pz) scalp electrodes, and the visual analogue scale for somnolence were recorded. Epicutaneous tests with histamine were performed, and serum H1-receptor antagonist concentrations were also measured. RESULTS: Neither cetirizine nor placebo significantly increased the mean P300 latency or somnolence as recorded on the visual analogue scale compared with predose baseline (P > .05), although increases were seen in some subjects after each of these treatments. Hydroxyzine and diphenhydramine increased the mean P300 latency and somnolence significantly (P < .05) compared with baseline; increases were observed in most, but not all subjects. Hydroxyzine increased P300 latency and somnolence significantly compared with placebo and with cetirizine. Diphenhydramine increased somnolence significantly compared with placebo. Overall, correlation between the objective test, P300 latency, and the subjective assessment, somnolence as recorded on the visual analogue scale, was statistically significant but clinically unimportant. Identification of central nervous system adverse effects after one potentially sedating H1-receptor antagonist did not predict central nervous system adverse effects after the others. CONCLUSIONS: Inter-individual objective and subjective central nervous system responses to H1-receptor antagonists are wide-ranging. The subjective responses can be misleading and do not necessarily predict the abnormalities that can be documented objectively after the same H1-receptor antagonist or a different H1-antagonist.

Adolescent↗
PubMed1977

Some observations on the antihistamine activity in the guinea pig of aliphatic 2,4-diketones, a new class of physiological tissue components.

Eight saturated aliphatic 2,4-diketones, ranging in chain length from C7 to C21 were examined for their potency in counteracting the effects of histamine anaphylaxis in guinea pigs. A 0.2% suspension of the mixed C15, C17, C19 and C21 diketones was more effective than a 1% phenylephrine solution when these were administered as aerosols. Of the individual diketones, 2,4-nonadecanedione was the most potent in vivo. ED50 data for the antihistamine activity of the C7, C9, and C13 homologues in the in vitro guinea pig ileum bioassay indicated that, on a weight basis, the activity increased with increasing molecular weight. The antiallergic activity of tissue and of urine extracts has been attributed to the presence of 2,4-diketones.

Anaphylaxis↗
PubMed1996

Characterization of the ocular antiallergic and antihistaminic effects of olopatadine (AL-4943A), a novel drug for treating ocular allergic diseases.

Olopatadine (AL-4943A; KW-4679) [(Z)-11-[3-(dimethylamino)propylidene]-6, 11-dihydrodibenz[b,e]oxepine-2-acetic acid hydrochloride] is an antiallergic/antihistaminic drug under development for topical ocular use. The effects of the compound on release of proinflammatory mediators (histamine, tryptase and prostaglandin D2) from monodispersed human conjunctival mast cells were assessed. Histamine receptor subtype binding affinities and functional potencies were determined with ligand binding and phosphoinositide turnover assays, respectively. Olopatadine inhibited the release of histamine, tryptase and prostaglandin D2, in a concentration-dependent manner (IC50 = 559 microM). Evaluation of the interaction of olopatadine with histamine receptors revealed a relatively high affinity for the H1 receptor (Ki = 31.6 nM, pKi = 7.5 +/- 0.1, n = 7) but lower affinities for H2 receptors (Ki = 100 microM, pKi = 4.0 +/- 0.19, n = 7) and H3 receptors (Ki = 79.4 microM, pKi = 4.1 +/- 0.16, n = 7). The H1 selectivity of olopatadine was superior to that of other ocularly used antihistamines studied, such as ketotifen, levocabastine, antazoline and pheniramine. The profiling of olopatadine in 42 nonhistamine receptor binding assays revealed that olopatadine interacts with only two nonhistamine receptor/uptake sites to any significant degree (pIC50 < or = 5-6). Olopatadine inhibited histamine-induced phosphoinositide turnover in human conjunctival epithelial cells (IC50 = 10 nM, pIC50 = 8.0, n = 4) and in other human ocular cells (IC50 = 15.8-31.6 nM, pIC50 = 7.5-7.8) and exhibited apparent noncompetitive antagonist properties in these cells, with an estimated dissociation constant (Kb) of 19.9 nM (pKb = 7.7, n = 6). This combination of mast cell mediator release inhibition and selective H1 receptor antagonism suggests that olopatadine may be particularly useful in the treatment of ocular allergic diseases. Indeed, olopatadine has recently shown clinical efficacy in an allergic conjunctivitis model in human subjects.

Anti-Allergic Agents↗
PubMedDate not supplied

[Perennial rhinitis: antihistaminic and anti-inflammatory treatment].

The use of various medications in chronic rhinitis in children is discussed. Evastin has been shown to eliminate histamine papules in 93% of cases and those caused by D. pteronyssinus in 68% of cases. After 10 days of treatment, conjunctival response decreased or disappeared in 80% of cases and nasal response decreased in 69%. Clinically, evastin was effective in 14 of 22 children and produced moderate effects in 2 and no effect in 6. There were no dropouts because of problems of tolerance. In a preliminary study of intranasal azelastin in 21 children with chronic allergic rhinitis, clinical improvement was significant. Various multicenter trials are reported, focusing on those using fluid budesonide. Both medications were effective in reducing symptoms and the antihistamine effect usually was earlier. There were no differences between medications as evaluated by nasal challenge or tolerance. Finally, budesonide was used in 13 patients for 4 months. Nasal obstruction and secretion improved, and rhinomanometry results improved significantly.

Adolescent↗