The intracerebroventricular administration of carbachol chloride induced a characteristic wet dog shake response in rats. Neither 5,6-dihydroxytryptamine, a serotonergic depletor, nor DL-p-chlorophenylalanine, an inhibitor of 5-HT synthesis, affected wet dog shakes induced by carbachol. Putative antiserotonergic drugs such as cyproheptadine, danitracen and pizotifen antagonized carbachol-induced wet dog shakes, but the 5-HT-receptor antagonist methergoline did not significantly affect the response. These results indicated that carbachol-induced wet dog shakes in rats are probably not related to increased activity of central serotonergic mechanisms. Additionally, the present experiments showed that the anticholinergic properties of the potent serotonergic blockers cyproheptadine, danitracen and pizotifen must be taken into account, and these drugs should be used with care as relatively selective pharmacological tools.
Comparison of the serotonin 5-HT2A receptor affinities of a parallel series of structural analogues of the novel ligand 9-aminomethyl-9,10-dihydroanthracene (AMDA) and a structurally similar prototypical tricyclic amine cyproheptadine suggests that the two agents bind to the receptor in different fashions. Examination of ligand-receptor model complexes supports the experimental data and suggests a potential origin for the differences in binding modes.
Pancreatic islet cell vacuolization, hyperglycemia, and glucose intolerance develop in rats after oral administration of cyproheptadine (CPH). In order to determine whether these effects were associated with abnormal insulin secretion, pancreas segments from CPH-treated and control rats were compared for their ability to secrete insulin in response to several stimuli. Oral administration of CPH (45 mg/kg/day) to rats for 1 or 8 days inhibited glucose-mediated insulin secretion from pancreas segments obtained 3 and 24 hr after the last dose of the drug. Insulin secretion had returned to normal by 48 hr after drug administration. Intraperitoneal administration of the drug was less effective than oral administration in inhibiting in vitro insulin secretion. Other stimuli for insulin secretion (tolbutamide, glucagon, L-leucine, and dibutyryl 3',5'cyclic AMP), like glucose, were incapable of releasing normal amounts of insulin from pancreas segments of CPH-treated rats. CPH and a metabolite, desmethyl-CPH, inhibited glucose-stimulated insulin secretion when added in vitro to pancreas segments from control rats. This suggests that the inhibition of insulin secretion in pancreas segments taken from animals treated with CPH could be due, at least in part, to the presence of drug and its metabolite in the tissue. A previously observed reduction in the pancreatic content of insulin in CPH-treated rats may also contribute to the abnormal insulin release in animals given the drug.
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Levocetirizine, the active enantiomer of cetirizine, is more potent and consistent than other popular H1 antihistamines for blocking the cutaneous response to histamine. These findings may predict the efficacy of this drug in treating allergic disorders.
Mast cells have been linked to rheumatoid arthritis (RA) and are essential to the pathogenesis of RA-like disease in a mouse model. We describe a 34-year-old woman who developed Sjögren's syndrome concurrently with telangiectasia macularis eruptiva perstans (TMEP), a rare form of cutaneous mastocytosis. The patient had sicca symptoms with an abnormal minor salivary gland biopsy and decreased salivary flow, peripheral neuropathy, an 80 pound weight loss, and a macular erythematous rash that exhibited superficial perivascular mast cell infiltrates on biopsy of lesional skin. This case further underscores the link between mast cells and the development of autoimmunity.
The association between adenoidal hypertrophy and rhinosinusitis with upper airway inflammation is increasingly recognized; however, no study has used magnetic resonance imaging (MRI) to assess the changes in adenoid size after medical treatment of rhinosinusitis.
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In patients with perennial allergic rhinitis, vitamin E supplementation (400 IU/d) did not have any significant effects on nasal symptom severity or on serum concentrations of specific IgE to 5 common allergens.
Loratadine syrup disrupted normal urethral development in the mouse, based on gross morphology and histological assessment, and also disrupted steroid receptor expression, producing an expression profile similar to that resulting from in utero exposure to ethinyl estradiol.
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In total, 20 adult Sprague-Dawley rats were used in this study. An ovalbumin-induced allergic rhinitis model was formed in three study groups except for the control group. Bosentan (100 mg/kg/day) was given to the bosentan-treated group for 7 days and desloratadine (10 mg/kg/day) was administered to the antihistaminic-treated group for 7 days. Nasal symptom scorings and histopathological examinations of the nasal tissues were carried out. Serum IgE levels and ET-1 and TNF-alpha mRNA expression levels were analysed. Between group comparisons for nasal symptoms, histopathological analysis, and molecular analyses were performed with a one-way ANOVA and Duncans multiple comparison tests. Significance was accepted at p smaller than 0.05.
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Limited information is available regarding sedation and motor function following repeat dosing of antihistamines. This study examined how promethazine and loratadine affect day-time drowsiness, the commencement of voluntary movement, and involuntary movement when administered on consecutive days.
The effects of third ventricle (3V) infusion of exogenous monoamines on the secretion of LH were investigated in Nembutal-blocked proestrous rats after electrochemical stimulation (ECS) of the medial preoptic area (MPOA). Two microcannulae were anatomically oriented through the ventral surface of the brain to establish a push-pull flow system in the 3V at the rate of 3.9 microliter/min for 160 min. Serotonin perfusions (2.6 x 10(-3) M for 160 min at 3.9 microgram/min) significantly depressed the MPOA-ECS-induced rise in plasma LH at 160 and 200 min, but did not diminish the secretion of LH after an intraatrial injection of 250 ng LRH. Seemingly, the reduced plasma LH which follows MPOA-ECS in serotonin-treated rats is the consequence of decreased hypothalamic LRH secretion. Desipramine (3.6 x 10(-4) M), a norepinephrine (NE) uptake inhibitor, did not prevent serotonin inhibition. In contrast, the specific serotonin uptake inhibitor. Lilly 110140 (3.2 X 10(-4) M), and cyproheptadine (2.9 x 10(-4) M) blocked the inhibitory effects of serotonin. Serotonin was also tested in proestrous rats anesthetized with Nembutal within 1 h after the beginning of the light cycle (morning rats) and in proestrous rats at least 15 min after the start of the dark cycle (night rats). Serotonin (2.6 x 10(-3) M) failed to diminish the rise in plasma LH after ECS in morning rats, but depressed the ECS-induced increase of LH in night rats. Perfusions of 3 X 10(-8) M NE at 3.9 microliter/min for 160 min augmented the plasma LH increase after MPOA-ECS but only at 160 and 200 min, while its response to LRH was not tested. At higher concentrations, 3 x 10(-6) M NE markedly suppressed the rise in plasma LH after ECS and also depressed the secretion of LH after an intraatrial injection of LRH. In contrast, 3 x 10(-6) M epinephrine which inhibited the response to LRH, potentiated the MPOA-ECS-induced rise in plasma LH. Higher concentrations of epinephrine (3 x 10(-4) M), however, inhibited both the ECS and LRH-induced secretion of LH.
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Release of plasma ACTH- and beta-endorphin (beta-EP)-like immunoreactivity (LI) was studied in vivo in a patient with an ectopic ACTH-producing malignant thymoma. Administration of lysin vasopressin stimulated concomitant release of plasma ACTH- and beta-EP-LI. Administration of cyproheptadine, naloxone, and somatostatin significantly suppressed plasma levels of ACTH- and beta-EP-LI, while saline infusion did not. Gel exclusion chromatography of the plasma extracts revealed that ACTH-LI consisted of two components, large and small molecular weight form, while beta-EP-LI consisted of three components, large molecular weight, beta-lipotropin-, and beta-EP-sized form; each of these components was incompletely suppressed by somatostatin infusion. It is suggested that certain tumors may have acquired aberrant multiple receptors during malignant transformation which may lead to the paradoxical hormone response as demonstrated in this case.
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Rats pretreated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, 10 micrograms/kg) are supersensitive to the edemagenic effects of carrageenan and dextran as indicated by the increased potency of these irritants in TCDD-treated animals compared to controls. This effect of TCDD was characterized using indomethacin, dexamethasone and a combination of cyproheptadine and pyrilamine as inhibitors of edema formation. Because TCDD increases the potency of carrageenan and dextran, it was necessary to select appropriate doses of the edemagenic irritants in order to evaluate the effect of edema inhibitors properly. At low and moderate irritant doses, TCDD-treated and control rats exhibited similar responses to inhibitory agents, suggesting that the mechanisms by which carrageenan and dextran produce edema involve the same mediators in control and TCDD-treated animals. The effect of TCDD on edema induced by bradykinin, histamine, prostaglandin E2 and serotonin, substances which are postulated endogenous mediators of carrageenan-, dextran- and/or compound 48/80-induced edemas, was also examined. Inasmuch as TCDD increased the edemagenic potency of bradykinin and histamine, but not that of prostaglandin E2 or serotonin, it was concluded that TCDD enhances carrageenan-, dextran- and compound 48/80-induced edema formation by augmenting the edemagenic activities of bradykinin and histamine. It is postulated that the mechanism of enhancement may involve TCDD-induced potentiation of the ability of bradykinin and histamine to stimulate phospholipase activity in vascular endothelial cells.
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Prazosin is recommended for treatment of Posttraumatic Stress Disorder (PTSD)-associated nightmares. Level A. Image Rehearsal Therapy (IRT) is recommended for treatment of nightmare disorder. Level A. Systematic Desensitization and Progressive Deep Muscle Relaxation training are suggested for treatment of idiopathic nightmares. Level B. Venlafaxine is not suggested for treatment of PTSD-associated nightmares. Level B. Clonidine may be considered for treatment of PTSD-associated nightmares. Level C. The following medications may be considered for treatment of PTSD-associated nightmares, but the data are low grade and sparse: trazodone, atypical antipsychotic medications, topiramate, low dose cortisol, fluvoxamine, triazolam and nitrazepam, phenelzine, gabapentin, cyproheptadine, and tricyclic antidepressants. Nefazodone is not recommended as first line therapy for nightmare disorder because of the increased risk of hepatotoxicity. Level C. The following behavioral therapies may be considered for treatment of PTSD-associated nightmares based on low-grade evidence: Exposure, Relaxation, and Rescripting Therapy (ERRT); Sleep Dynamic Therapy; Hypnosis; Eye-Movement Desensitization and Reprocessing (EMDR); and the Testimony Method. Level C. The following behavioral therapies may be considered for treatment of nightmare disorder based on low-grade evidence: Lucid Dreaming Therapy and Self-Exposure Therapy. Level C No recommendation is made regarding clonazepam and individual psychotherapy because of sparse data.
Recently, it is claimed that the usage of the intranasal glucocorticosteroids alone, instead of H1-antihistamines + intranasal glucocorticosteroids, reduces the complaints in moderate-to-severe seasonal allergic rhinitis (SAR). This study aims to evaluate the efficacy of the intranasal glucocorticosteroids alone during the pollen season by using objective and subjective parameters. Twenty-four patients (mean age, 12.17 +/- 2.26 years) with SAR sensitive to pollen are included in this study. The patients were divided into two groups randomly. Twelve patients in group I were given H1-antihistamine (loratadine) + intranasal glucocorticosteroid (mometasone furoate), and 12 patients in group II were given only intranasal glucocorticosteroid (mometasone furoate) for 12 weeks. To evaluate the results, subjective parameters (daytime nasal symptoms score, daytime eye symptoms score, and nighttime symptoms score) and objective parameters (nasal smear, nasal peak inspiratory flow [NPIF], and nasal biopsy) are used. With regard to the baseline data, it was observed that both groups had a significant decrease in total symptom score (p < 0.01), a significant increase in NPIF values (p < 0.01), and a significant decrease in the number of eosinophils in both nasal smear and biopsy (p < 0.01) after treatment. Comparing groups I and II in terms of treatment success, the improvement in daytime nasal symptoms score (p < 0.01 versus p < 0.01), daytime eye symptoms score (p < 0.01 versus p < 0.01), and total symptom score (p < 0.versus p < 0.01) was not different. However, there was a significant improvement in nighttime symptoms score between groups I and II (p < 0.01 versus p > 0.05). Furthermore, NPIF and nasal biopsy findings did not differ between groups (p > 0.05). The usage of H1-antihistamine + intranasal glucocorticosteroid has no superiority over the administration of intranasal glucocorticosteroid alone for treatment of SAR in pollen season. However, this finding needs to be confirmed in larger series studies.
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The influence of various 5-hydroxytryptaminergic agonist and antagonist drugs on body-temperature response to cobaltous chloride in mice was noted. Pretreatment with p-chloroamphetamine, p-chlorophenylalanine, and p-iodoamphetamine antagonized the body-temperature response to cobalt. p-Chloroamphetamine and p-chlorophenylalanine reduced, while p-iodoamphetamine elevated, brain serotonin levels. The uptake inhibitor agents, fluoxetine and nisoxetine, failed to modify the ability of p-chloroamphetamine to antagonize cobalt hypothermia. Cyproheptadine, methergoline, and xylamidine pretreatment enhanced rather than antagonized body-temperature depression by cobalt. Tryptophan hydroxylase inhibitors antagonized cobalt hypothermia, but receptor-blocking agents were without influence, indicating that antagonism was mediated through mechanisms other than the depletion of serotonin. Elevation rather than depletion of brain serotonin by p-iodoamphetamine and failure of uptake inhibitors to modify p-chloroamphetamine antagonism of cobalt hypothermia lend further support for a nonserotonergic role of these amines in their ability to antagonize body-temperature depression by cobaltous chloride in mice.
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Thirty-five patients with moderate-to-severe asthma, most receiving inhaled steroids, were enrolled in this double-blind, crossover study. In addition to their maintenance therapy patients received either loratadine, 20 mg once daily, or placebo for 4 weeks before crossing over to the other preparation for a further 4 weeks. Variables of efficacy were daily and nocturnal respiratory symptoms, lung function (PEF, FEV1, FVC), and bronchodilator use.
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Influence of GABA onlocomotor activity and gross behavior of mice, rats, and rabbits was studied. In mice and rats, IP GABA injection produced decreased locomotor activity, but in rats and rabbits head twitches and disturbances in body balance were seen. GABA-induced head twitches were inhibited by picrotoxin, clonidine, morphine, or cyproheptadine. Our results suggest a serotonergic component in GABA-induced head twitches, but it is not the only mechanism involved in this behavior.
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This study investigated the additive effects of concomitant montelukast and loratadine when compared with montelukast, loratadine, and inhaled beclomethasone monotherapies in asthma. Methods. Patients (N = 406) were 15 to 65 years of age with a forced expiratory volume in 1 second (FEV(1))-predicted of 50% to 85%, FEV(1) reversibility > or = 15%, and a minimal level of daytime symptoms and beta -agonist use. This three-part 2X2 crossover-study consisted of two double-blind 6-week treatment periods where patients were administered once daily oral montelukast 10 mg, loratadine 10 mg, montelukast 10 mg + loratadine 10 mg, or twice daily inhaled beclomethasone 200 mu g. A subsequent 48-week extension study compared montelukast + loratadine with beclomethasone. The primary endpoint was the percentage change from baseline in FEV(1).
A survey of novel small-molecule therapeutics reveals that the majority of them result from analogue design and that their market value represents two-thirds of all small-molecule sales. In natural science, the term analogue, derived from the Latin and Greek analogia, has always been used to describe structural and functional similarity. Extended to drugs, this definition implies that the analogue of an existing drug molecule shares structural and pharmacological similarities with the original compound. Formally, this definition allows the establishment of three categories of drug analogues: analogues possessing chemical and pharmacological similarities (direct analogues); analogues possessing structural similarities only (structural analogues); and chemically different compounds displaying similar pharmacological properties (functional analogues).
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Intracerebral (i.c.) injection of serotonin (5-HT) into mice induced head twitches in a dose-dependent manner at 10 min after injection. The head twitches induced by 5-HT (i.c.) were potentiated by the pretreatment of isocarboxazid (3 mg/kg i.p.), and inhibited by cyproheptadine (0.3 mg/kg i.p.), a 5-HT antagonist. Benzodiazepines such as fludiazepam and diazepam potentiated the head twitches induced by 5-HT (i.c.) in a dose-dependent manner. Mescaline (50 mg/kg i.p.) also induced head twitches in mice at 15 and 30 min after injection. Benzodiazepines potentiated the head twitches induced by mescaline in a dose-dependent manner. Cyproheptadine blocked the potentiating effect of benzodiazepines on the head twitches induced by both 5-HT (i.c.) and mescaline. By repeated administration of fludiazepam or diazepam for 5 days, the potentiating effect of both drugs on the head twitches induced by mescaline was unchanged and their anticonvulsant effects were not modified. In contrast, the potency of both drugs on muscle relaxation was significantly decreased by repeated administration. Benzodiazepines failed to change the uptake of 5-HT into the synaptosomal fractions from the rat brain. These results suggest that the pharmacological action of benzodiazepines is derived at least in part from their activating effect on 5-HT receptors.
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A randomized, double blind, parallel-group, placebo-controlled study was carried out in patients aged older than 12 years with PER. Main inclusion criteria were: instantaneous total symptom score (i6TSS) >or=45, nasal obstruction score or=2 as moderate during the first visit. The primary efficacy endpoint was the 12-week average change from baseline of the patients' i6TSS.
Crinum glaucum A. Chev (Amaryllidaceae) (CG) is a bulbous plant widely used in folk medicine in the treatment of cough, asthma and convulsions. This study was carried out to investigate the anticonvulsant, anxiolytic and hypnotic effects of the aqueous bulb extract of C. glaucum and its possible mechanism (s) of action. The anticonvulsant activity of C. glaucum extract (400-1200 mg kg(-1) p.o.) was investigated using picrotoxin, strychnine, isoniazid, pentylenetetrazol and N-methyl-D-aspartate (NMDA)-induced seizures in mice while the elevated plus maze test (EPM) and hexobarbitone-induced sleeping time (HIST) were used to evaluate the anxiolytic and hypnotic effects, respectively. Animals were pretreated with flumazenil (3 mg kg(-1); i.p. GABA(A) receptor antagonist), cyproheptadine (4 mg kg(-1); i.p. 5-HT2 receptor antagonist), L-arginine (500 mg kg(-1); p.o. Nitric Oxide (NO) precursor) and L-Nitroarginine (L-NNA) (10 mg kg(-1) i.p. Nitric Oxide Synthase (NOS) inhibitor) were used to investigate the probable mechanism (s) of anticonvulsant activity. Oral administration of CG significantly (p < 0.001) delayed the onset of seizures induced by picrotoxin, strychnine, isoniazid and pentylenetetrazol with peak effect at 1200 mg kg(-1) in comparison to control groups. CG (800 and 1200 mg kg(-1)) strongly antagonized NMDA-induced turning behavior. Pretreatment of mice with cyproheptadine could not reverse the anticonvulsant effect of CG. However, pretreatment with flumazenil and L-NNA significantly (p < 0.05) reversed the anticonvulsant effect of CG while L-arginine pretreatment significantly (p < 0.001) delayed the onset of seizures when compared with control and extract (1200 mg kg(-1) only). CG potentiated hexobarbitone-induced sleeping time with peak effect at 400 mg kg(-1) and also significantly (p < 0.05) increased open arm exploration in EPM and had its peak anxiolytic effect at 100 mg kg(-1). The data obtained suggests that aqueous bulb extract of Crinum glaucum possess anticonvulsant, anxiolytic and hypnotic activities which involve an interaction with GABAergic, nitrergic and glutaminergic systems to exert its effects.