Disease relevance of Chlo-amine

• Effect of the antihistaminic agents meclastine and dexchlorpheniramine on the response of human growth hormone to arginine infusion and insulin hypoglycemia [1].
• In comparative studies in patients with seasonal rhinitis it has been shown to be of similar efficacy as intranasal flunisolide and intranasal beclomethasone dipropionate and superior to intranasal sodium cromoglycate (cromolyn sodium) and the antihistamine dexchlorpheniramine [2].
• KW1070, a new aminoglycoside antibiotic with the novel aminocyclitol, fortamine, has a broad spectrum of activity in vitro and in vivo against gram-positive and gram-negative bacteria [3].
• Twenty-one children received loratadine 0.11-0.24 mg/kg ideal body weight once daily and 19 dexchlorpheniramine 0.10-0.23 mg/kg every 8 h (0.30-0.69 mg/24 h) for 14 consecutive days [4].
• At a dose ineffective per se, dexchlorpheniramine (10 mg/kg i.p.) antagonized the hyperalgesia induced by HTMT (40 mug/mouse i.c.v. or 10 mg/kg s.c.). Dimaprit (H(2) receptor agonist, 30 mg/kg i.p.) and ranitidine (H(2) receptor antagonist, 20 and 40 mg/kg i.p.) reduced the nociceptive responses in the early and late phases [5].

Psychiatry related information on Chlo-amine

• Repeated-dose effects of mequitazine, cetirizine and dexchlorpheniramine on driving and psychomotor performance [6].
• Conversely, intraperitoneal (ip) injection of dexchlorpheniramine (30 and 40 mg/kg) and diphenhydramine (20 and 40 mg/kg) increased the pain threshold in both tests [7].

High impact information on Chlo-amine

• Prednisolone, dexchlorpheniramine, and ranitidine were standard premedication [8].
• The binding of 125I-iodobolpyramine to human T cells was reversible when using 1000-fold excess of the cold H1 antagonist, d-chlorpheniramine [9].
• Two H1 antagonists, dexchlorpheniramine (10 mg, iv) and promethazine (50 mg, im), reduced PRL release in both sexes, stimulated LH release in men, and inhibited LH release in women [10].
• In order to evaluate the possible role of endogenous histamine in the control of human growth hormone (hGH) secretion, we investigated the effect of two anti-histamine drugs, meclastine and dexchlorpheniramine, on the hGH response to arginine infusion and to insulin hypoglycemia in 30 normal subjects [1].
• The results from activation study using visual discrimination tasks demonstrated that enhanced activity in the right prefrontal and anterior cingulate cortices as well as a decreased activity in the left temporal and frontal cortices and midbrain after the treatment of d-chlorpheniramine [11].

Chemical compound and disease context of Chlo-amine

• The study indicated that dexchlorpheniramine at the doses tested, was significantly more effective in controlling hay fever symptoms than terfenadine [12].
• Both patients had a history of eczema that worsened following the ingestion of the antihistamine Polaronil (dexamethasone/dexchlorpheniramine) [13].
• Mequitazine and dexchlorpheniramine in perennial rhinitis. A double-blind cross-over placebo-controlled study [14].
• A slow release combined preparation (dexchlorpheniramine + pseudoephedrine) for symptomatic treatment of the common cold [15].

Biological context of Chlo-amine

• 3. DH in doses of 0.1, 1.0 and 10 mg kg(-1) and CP in doses of 0.01, 0.1 and 1.0 mg kg(-1) administered intravenously 15 min after the OA challenge partially reduced the UNDW-IB at 1 and 2 min after the UNDW inhalation in a dose-dependent manner [16].
• Auditory event-related potentials (ERPs) were recorded in 20 healthy male humans, who received either a single 4 mg dose of d-chlorpheniramine or a placebo, according to a double-blind design [17].
• Dexchlorpheniramine even enhanced the apomorphine-induced penile erections and induced penile erections in physostigmine-treated rats [18].
• Amylin's inhibitory effect on food intake (i.e. 50% reduction in cumulative food intake 30 min after ingestion) was markedly reduced by CPA and PYR (e.g. amylin and CPA: 5% reduction versus control) [19].
• The results showed that the amination at position 4 in fortamine occurred after formation of the pseudodisaccharide [20].

Anatomical context of Chlo-amine

• The first-generation histamine H1-receptor antagonists, chlorpheniramine (CPHE) and diphenhydramine (DPH), may activate histamine release from basophils and mast cells [21].
• Based on this premise, the objective of the present study was to compare HA with the H1-receptor antagonist d-chlorpheniramine (CPR) in effects on reinforcement and memory parameters after injection into different subregions of the rat nucleus accumbens (NAcc) [22].
• FG 7051, FG 7052 and dexchlorpheniramine were weak 5HT antagonists on the rat ileum but potentiated the pressor responses to 5HT; the most potent uptake inhibitor, FG 7051, was the strongest potentiator [23].
• A double-blind cross-over study was performed in 12 healthy female volunteers comparing cetirizine di-HCl (10 mg) and sustained release dexchlorpheniramine maleate (6 mg) with respect to attentuation of histamine-induced skin wheals and subjective central nervous system (CNS) effects [24].
• Both hydroxyzine and D-chlorpheniramine crossed the blood-brain barrier in significant amounts [25].

Associations of Chlo-amine with other chemical compounds

• Development of a validated capillary electrophoresis method for enantiomeric purity testing of dexchlorpheniramine maleate [26].
• The radioactivity in the brain was significantly reduced by intravenous pretreatment with d-chlorpheniramine (5 mg), a histamine H1 antagonist [27].
• RESULTS: Dexchlorpheniramine and mequitazine significantly impaired driving performance on the highway driving test on the first day; dexchlorpheniramine increased Standard Deviation of Lateral Position by 2 cm [95% confidence interval (CI) 0.5, 3.8] and mequitazine by 2.5 cm (CI 1.0, 4.3) [6].
• Stereoisomers of chlorpheniramine inhibited [(3)H]mepyramine binding; d-chlorpheniramine inhibited more potently than l-chlorpheniramine, K(i) values being 1.1 +/- 0.4 and 270 +/- 170 nM, respectively [28].
• Treatment of seasonal allergic rhinitis--a double blind, group comparative study of terfenadine and dexchlorpheniramine [29].

Gene context of Chlo-amine

• Promethazine, given concomitantly to an iv bolus injection of TRH (200 micrograms) (6 women) and d-chlorpheniramine, given at the onset of suckling (6 women), did not alter stimulation of PRL release induced by these challenges [30].
• There were no changes in global CBF for the subjects treated with 2 mg d-chlorpheniramine (pre; 44.8+/-3.3 ml dl(-1) min(-1) vs post; 44.4+/-4.7 ml dl(-1) min(-1)) [11].
• The regional blockade of H1R was observed mainly in the frontal, temporal and anterior cingulate cortices, and the intravenous administration of d-chlorpheniramine as a therapeutic dose (2 mg) blocked over 60% of H1R in the frontal cortices [11].
• The safety and efficacy of loratadine was compared with that of dexchlorpheniramine in children with allergic rhinitis [4].
• Addition of the H1-receptor antagonist, d-chlorpheniramine, to the perfusate completely inhibited basal histamine release from the IPL of both air- and O2-exposed rats, while addition of the H2-receptor antagonist, metamide, potentiated the release process [31].

Analytical, diagnostic and therapeutic context of Chlo-amine

• Subjects reported to be less alert after treatment with dexchlorpheniramine [32].
• Regional CBF was measured by the radioactive microspheres technique 15 min after each injection of d-chlorpheniramine or saline [33].
• The aim of this study was to visualize the brain mechanism of impaired visuomotor spatial cognition with orally administered d-chlorpheniramine, a first-generation sedative antihistamine, using H(2) (15)O and positron emission tomography (PET) [34].
• Normal subjects were randomly assigned to two groups (chlorpheniramine and placebo) and performed a spatial discrimination task after the oral administration of 6 mg d-chlorpheniramine or a placebo [34].
• METHODS: At the end of the surgery, patients in the study group (n = 30) were given an intramuscular injection of 40 mg DM and 20 mg chlorpheniramine (CPM) while in the study group (n = 30), the patients were given intramuscular 20 mg CPM only [35].

References