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Clonidine exhibited a dose-dependent protection against harmine-induced tremors in mice. This protective effect was not completely blocked by pretreatment with yohimbine. The serotoninergic (5-HT) agonist quipazine and the uptake inhibitor fluoxetine completely antagonized this effect. On the other hand, the 5-HT antagonist cyproheptadine potentiated the protective effect of sub-effective doses of clonidine. These observations suggest a serotonin-mediated action of clonidine in its antitremor action against harmine-induced tremors.
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We extended a previous study that had shown the selective D1 receptor antagonist SCH 23390, at relatively high doses, to stimulate prolactin (PRL) secretion in the rat and weakly inhibit [3H]spiperone binding to striatum and anterior pituitary (AP) membranes. No specific [3H]SCH 23390 binding sites, up to the micromolar range, were detected in rat AP while specific, saturable [3H]SCH 23390 binding sites (low nanomolar range) were observed in the striatum. In vivo SCH 23390 (1 mg/kg s.c.) induced higher plasma PRL levels, not reversible by the D1 agonist SKF 38393. Similarly the postsynaptic serotonin (5-HT) antagonists metergoline and cyproheptadine did not influence the SCH 23390 effect on PRL. SCH 23390 was also unable to antagonize the decrease of PRL secretion induced by the selective D2 agonist LY 171555. However this latter compound prevented SCH 23390 as well as sulpiride from increasing the PRL concentrations above the control values. These data rule out the possibility that D1 or 5-HT receptors mediate the stimulation of PRL release by SCH 23390. This effect is more likely to be due to a weak indirect interaction with AP-D2 receptors, as indicated by the non-competitive inhibition of [3H]spiperone binding to AP exerted by SCH 23390. Alternatively, non-specific mechanisms triggered by the multiple behavioral changes elicited by such high doses of SCH 23390 may be involved.
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To assess whether fexofenadine in a range of doses from 80 to 180 mg has any disruptive effects on aspects of psychomotor and cognitive function in comparison with placebo, loratadine and promethazine, an antihistamine known to produce psychomotor and cognitive impairment.
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Patients were randomly allocated to double-blind treatment with intranasal beclomethasone 200 mu g/twice daily (study 1 only), placebo, montelukast 10 mg+loratadine 10 mg, montelukast 10 mg, or loratadine 10 mg once daily. The primary endpoint was the Composite Symptom Score (CSS): average of daily diary scores for Daytime Nasal Symptoms and Nighttime Symptoms.
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To investigate whether PAF could stimulate human mast cell mediator release and whether rupatadine (RUP), a dual histamine-1 and PAF receptor antagonist, could inhibit the effect of PAF on human mast cells.
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The pro-inflammatory tigliane esters 12-deoxyphorbolphenylacetate (12-DOPPA) and 12-deoxyphorbolphenylacetate-20-acetate (12-DOPPAA) at a dose of 0.1 microgram induced erythema in the mouse ear. Observations of ear redness were made both two and four hours after application. Indomethacin was only partly successful as an antagonist since 10% inhibition of 12-DOPPA and no inhibition of 12-DOPPAA induced erythema was produced four hours after application. The free radical scavengers, phenol, thioanisole and sodium benzoate all produced less than 30% inhibition of 12-DOPPA induced erythema and less than 15% inhibition of 12-DOPPAA, whereas aminopyrine produced 70% and 25% inhibition of 12-DOPPA and 12-DOPPAA respectively. The fact that free radical scavengers (with the exception of aminopyrine) and indomethacin, failed to markedly change the mouse ear reaction to 12-deoxyphorbol esters, indicated that this erythema is not entirely mediated via cyclooxygenase products. Mepyramine and cyproheptadine also failed to inhibit the erythema, whereas hydrocortisone produced a 55% inhibition of the 12-DOPPA and a 20% inhibition of the 12-DOPPAA reaction. The membrane stabilising agents trifluoperazine, promethazine, imipramine and desmethylimipramine were the most successful compounds used in inhibiting both 12-DOPPA and 12-DOPPAA induced erythema. In addition propranolol, which inhibits stimulus activation of phospholipase A2, produced 70% and 55% inhibition of the reaction of mice ears to 12-DOPPA and 12-DOPPAA.
In order to assess the role of inflammation and its components in spontaneous cure of Strongyloides ratti infestation, rats were treated with non-steroid anti-inflammatory agents (indometacin; sodium salicylate) or with antagonists of certain mediators (dexchlorpheniramin; cyproheptadin, promethazin). Results were compared with those obtained in similar treatments of rats infested by other Nematoda which also give rise to spontaneous cure: especially Trichinella spiralis, and Nippostrongylus brasiliensis. Coordinating the various findings made it possible to devise a pattern accounting for the chain of reactions that lead to rejection of the parasite.
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Due to Mexico's complicated socioeconomic environment, causing a high occurrence of >1 person sharing a single room, respiratory conditions are spread easily. Respiratory conditions are the main reason for consultation with a physician. The most frequent symptoms are throat soreness and cough; therefore, a new formulation combining loratadine and ambroxol hydrochloride was designed to treat these 2 major symptoms. The combination is expected to provide relief when coprescribed with more specific therapies, such as antibiotics.
The CNS depressant effects of H1 antihistamines are promethazine approximately diphenhydramine > loratadine = placebo. Of the non-sedating antihistamines, loratadine was devoid of adverse cardiovascular effects whereas terfenadine caused a pronounced disruption of the normal ECG, characterized by a torsades de pointes-like effect.
Our previous study has proven that hypothalamic paraventricular nucleus (PVN) plays a role in antinociception. The effects of studied classical neurotransmitter on PVN antinociceptive modulation were investigated in the rat. The results showed: (1) Pain stimulation increased norepinephrine (NE), but not epinephrine, dopamine (DA), 3,4-dihydroxyphenylacetic acid (DA metabolic product), homovanilic acid (DA metabolic product), serotonin (5-HT), 5-hydroxyindoleacetic acid (5-HT metabolic product), acetycholine (Ach), choline (Ach metabolic product), gamma-aminobutyric acid (GABA), and L-glutamate acid concentrations in the PVN perfusion liquid; (2) PVN stimulation with L-glutamate sodium, which excited local neurons only, did not influence the concentrations of the studied classical neurotransmitter and metabolic product in the PVN perfusion liquid; (3) Microinjection of NE, epinephrine, or L-glutamate sodium into the PVN elevated pain threshold, and local administration of GABA decreased pain threshold in a dose-dependent manner, but PVN administration of Ach, DA, or 5-HT did not change pain threshold; (4) Microinjection of phentolamine (alpha-receptor antagonist) or MK801 [NMDA-receptor antagonist] into the PVN reduced pain threshold, and local administration of bicuculline (GABA-receptor antagonist) raised pain threshold, but PVN administration of propranolol (beta-receptor antagonist), atropine (Muscarinic cholinergic receptor antagonist), 6-OH gallamine (Nicotinic cholinergic receptor antagonist), fluperidol (DA-receptor antagonist), or cyproheptadine (5-HT-receptor antagonist) did not alter pain threshold. The data suggested that endogenous NE, not epinephrine, 5-HT, Ach, GABA, and L-glutamate acid played an important role in the PVN antinociceptive modulation.
Cetirizine acted earlier and was more effective than loratadine or placebo in reducing symptoms of seasonal allergic rhinitis in subjects undergoing a controlled pollen challenge, replicating results from an earlier, identically designed study, demonstrating reproducibility of these assessments by the EEU.
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The inhibitory effects of loratadine on nasal lavage fluid levels of alpha 2-macroglobulin suggest that histamine, through effects on microvascular H1-receptors, mediates allergen challenge-induced exudation of bulk plasma in acute allergic rhinitis. The reduced lavage fluid levels of tryptase suggest either that loratadine directly attenuates mast cell release activity or that loratadine, through inhibition of the exudation process, simply attenuates luminal entry of tissue solutes (in this case, tryptase).
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Treating patients with allergic rhinitis with montelukast sodium and loratadine were of similar effect. Histamine and leukotriene are both important inflammatory factors in the pathogenesis of allergic rhinitis and both play roles by affecting eosinophil accumulation and activation and by decreasing the formation of specific IgE. Leukotriene receptor antagonist is a new drug to treat allergic rhinitis.
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Nasal epithelial cells represent the first barrier against noxious agents and allergens. In allergic rhinitis, these cells are activated and histamine may be involved in this activation. Loratadine and one of its active metabolites, descarboethoxyloratadine, were studied for their ability to reduce the activation of nasal epithelial cells by histamine. Nasal turbinates or polyps were removed during surgery from 19 subjects, and nasal epithelial cells were recovered after enzymatic digestion. The in vitro activation of epithelial cells with histamine using an optimal dose (1 microM) and an optimal time (24 h) of incubation was studied, and the effect of loratadine or descarboethoxyloratadine (10 microM) was investigated. The expression of membrane markers (intercellular adhesion molecule-1 (ICAM-1) and a human leukocyte class II antigen (HLA-DR) was assessed by immunocytochemical analysis using an alkaline-antialkaline phosphatase (APAAP) system. The spontaneous expression of both markers was not significantly different in cells recovered from nasal turbinates or polyps, and there was a highly significant increase in the numbers of cells expressing ICAM-1 and HLA-DR following incubation with histamine. Loratadine or descarboethoxyloratadine significantly blocked these effects. This study shows a new possible antiallergic effect of H1-blockers and suggests that their effects on epithelial cells may be relevant in vivo.
Cachexia is a complex metabolic syndrome associated with many chronic or end-stage diseases, especially cancer, and is characterized by loss of muscle with or without loss of fat mass. The management of cachexia is a complex challenge that should address the different causes underlying this clinical event with an integrated or multimodal treatment approach targeting the different factors involved in its pathophysiology.
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The present studies tested the ability of 1,8-cineole to produce inflammatory oedema in the hind paw of the rat and verified the possible involvement of mast cells in the response. Subplantar injection of 1,8-cineole (10, 15 and 20 microl/paw) induced a dose-dependent paw oedema which was apparent within 30 min. At higher doses the oedema effect was persistent, peaked at 2 h, and then decreased gradually but was still pronounced at 24 h post injection. In contrast, the oedema produced by mast cell degranulator compound 48/80 (10 microg/paw) had a rapid onset with a peak effect at the first hour, followed by a gradual decrease thereafter and at 24 h post injection it was almost absent. The oedema response to 20 microl 1,8-cineole was significantly inhibited throughout its time-course in rats pretreated with antihistaminic and antiserotonergic drugs such as diphenhydramine, methysergide and cyproheptadine or with ketotifen, a mast cell stabilizer. A more effective blockade of the oedema response was, however, observed in rats depleted of mast cell granules by systemic treatment with compound 48/80. Furthermore, 1,8-cineole was able to cause rat peritoneal mast cell degranulation (94%) in vitro, in a concentration as low as 0.3 microl/ml, which was almost comparable to that produced by 0.1 microg/ml of compound 48/80. The data provide evidence of a key role for the mast cell in 1,8-cineole-induced hind paw oedema in the rat.
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Desloratadine is a non-sedating, long-acting histamine H(1) receptor antagonist indicated for the symptomatic relief of allergic rhinitis (AR) and chronic idiopathic urticaria in patients aged>12 years.
Montelukast alone, levocetirizine alone, desloratadine alone, and the montelukast/antihistamine combinations significantly improved nasal symptoms during the first 24 hours. Improvement gradually increased during the 6 weeks of treatment, especially in patients receiving montelukast alone or in combination therapy with the antihistamine in both arms. Improvement at 42 days of treatment was significantly greater than that achieved on the 1st day of therapy in patients treated with the combination of montelukast and levocetirizine.
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The 1996 Medical Expenditure Panel Survey Nursing Home Component (MEPS NHC), a survey of a nationally representative sample of NHs and residents.
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This study shows that ebastine in a 20-mg dose is an effective once-daily antihistamine. Superior efficacy was found in comparison to cetirizine (10 mg) or loratadine (10 mg) on the overall skin wheal response after single and multiple doses.
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Fluconazole inhibits CYP2C19. Citalopram is a substrate for 2C19 and inhibition of its metabolism may result in serotonin toxicity. Serotonin toxicity in oncology patients may not present with the classic constellation of signs typically described in the literature. Delirium may be the only presenting feature. Current level of evidence for treatment of serotonin toxicity is level 4 or 5 (case series and expert opinion). Nevertheless, there is a strong theoretical basis for treating serotonin toxicity in medical patients with a 5H(2A) blocker such as cyproheptadine.
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The teratogenic effect of cyproheptadine chlorhydrate was studied in Wistar rats. Rats were given the substance by gastric intubation on days 6-15 of pregnancy in two experimental series. In the first series rats were treated at doses of 25 and 50 mg/kg/d and in the second one they received 15, 25 and 35 mg/kg/d. Controls received only an equivalent volume of water by the same route. Doses of 25 or more mg/kg/d are highly embryotoxic. At 15 mg/kg/d the effects were relatively minor. The major anomalies caused by the drug were edema and abnormal ossification of the ribs. Some other malformations were also found: craniorrhachischisis, cleft lip, cleft palate, hypoplastic limbs, micrognathy, micromelia, and vascular damage.
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Desloratadine is approved for the treatment of symptoms associated with seasonal allergic rhinitis (SAR), perennial allergic rhinitis (PAR), and chronic idiopathic urticaria (CIU) in patients aged > or =12 years. In placebo-controlled trials, desloratadine demonstrated superior efficacy as a once-daily treatment of SAR, PAR, and CIU. Data suggest that desloratadine has antiinflammatory and decongestant activity.
To develop a liquid chromatography-tandem mass spectrometry (LC-MS/MS) method for the simultaneous determination of desloratadine and its metabolite 3-OH desloratadine in human plasma.
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Female NC/Jic mice were sensitized and challenged repeatedly at 48 h intervals for 10 and 30 days by painting 1% 2,4,6-trinitrochlorobenzene (TNCB) on both ears. Mice challenged with TNCB for 30 days developed an inflammatory dermatitis with high immunoglobulin E (IgE) titer. Histological analysis with acidic Toluidine Blue staining revealed that dermal mast cells markedly differentiated and intensely degranulated, consistent with a dramatic increase in scratching behavior. A significant increase in total scratching events could be observed in mice treated with TNCB for a short period of 10 days. Extending the term of TNCB application to 30 days, the IgE titer and number of mast cells elevated significantly, and thus various drugs were evaluated pharmacologically by using the mice treated with TNCB for 30 days. Terfenadine and cyproheptadine attenuated the chronic scratching behavior. Tacrolimus and dexamethasone were less effective and cromolyn showed no effect. In addition, terfenadine and tacrolimus suppressed the degranulation of mast cells. The present chronic scratching model could be suitable to evaluate drugs effective for suppression of mast cell differentiation and degranulation by irritation, and may represent a promising tool to develop new drugs for inflammatory pruritus associated with, for example, atopic dermatitis.
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Febrile neutropenia is an oncologic emergency that can result in serious consequences. Granulocyte colony stimulating factors (G-CSFs) are often used as prophylaxis for febrile neutropenia. Bone pain is the most notorious adverse effect caused by G-CSFs. Specifically, with pegfilgrastim (Neulasta(®)), the incidence of bone pain is higher in practice than was observed during clinical trials. Traditional analgesics, such as non-steroidal anti-inflammatory drugs (NSAIDs) and opioids, can be ineffective in severe pegfilgrastim-induced bone pain. With the high frequency of this adverse effect, it is clear that health practitioners need additional treatment options for patients who experience severe pegfilgrastim-induced bone pain. The mechanisms of bone pain secondary to G-CSFs are not fully known, but research has shown that histamine release is involved in the inflammatory process. There is scant previous clinical data on antihistamine use in the management of G-CSF-induced pain. We present the first case report in which loratadine prophylaxis completely alleviated NSAID-resistant severe pain secondary to pegfilgrastim. The result showed that loratadine may be a promising option for severe, resistant pegfilgrastim-induced bone pain. Further clinical studies are warranted and ongoing.