Relevant bibliographies by topics / Serotonin Antihistamines

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Academic literature on the topic 'Serotonin Antihistamines'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Serotonin Antihistamines"

1

Dukhanin, Alexander S. "Pharmacological profile of antihistamines: focus on unwanted drug interactions." Russian Journal of Allergy 17, no. 4 (January 29, 2021): 46–56. http://dx.doi.org/10.36691/rja1407.

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Differences between individual antihistamines are determined by such pharmacokinetic properties as the rate and completeness of absorption, half-life, the participation of hepatic and renal mechanisms of elimination from the body. Pharmacodynamic features of the antihistamine include selectivity and affinity for histamine H1-receptors and the presence of central effects. The mechanisms of the development of unwanted drug interactions with second-generation antihistamines are analyzed in detail. Three levels of interaction have been identified: 1) hepatic enzymes of the P450 system; 2) membrane carriers of organic anions (OATP) transport proteins on the sinusoidal membrane of hepatocytes and the luminal membrane of the epithelium of the proximal nephron tubule; 3) P-glycoprotein (Pgp, ABCB1-protein) of epithelial cells of the small intestine the area of absorption of oral forms of antihistamines, the epithelium of the proximal tubule and the BBB (blood-brain barrier). The emphasis is made on the description of the dependence of the pharmacological profile of antihistamines on its chemical structure. The elasticity of the bilastine molecule, the ability to induce a change in conformation underlies the high complementarity of bilastine to the recognition site of the H1-receptor which is a high affinity. Experimental evaluation confirms this conclusion: the dissociation constant (Dс) of the bilastin-receptor complex is in the nM concentration range. The bilastine molecule, as a representative of antihistamines with zwitterionic properties, carries both a positive and a negative charge at a physiological pH, making it difficult for its penetration into the brain. The peculiarities of the chemical nature of the bilastine molecule are reflected in the specific pharmacological profile of AGP. In vitro studies have shown a high specific affinity of bilastine for H1-receptors with a very low affinity for other histamine receptors (H2, H3, H4), serotonin, bradykinin, muscarinic and adrenergic receptors). According to this indicator, bilastine is 3 times higher than cetirizine and 5 times higher than fexofenadine. Bilastine is practically not metabolized in the body and is excreted mainly unchanged, and also does not have a cardiotoxic effect. Bilastine is well tolerated; as a therapeutic dose it has a less pronounced sedative potential compared to other second-generation antihistamines.
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2

Winters, Tammy A., and Barbara L. Slifer. "Discriminative stimulus properties of antihistamines may involve mediation by serotonin." Pharmacology Biochemistry and Behavior 32, no. 4 (April 1989): 1087. http://dx.doi.org/10.1016/0091-3057(89)90127-5.

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3

Yeh, S. Y., C. Dersch, R. Rothman, and J. L. Cadet. "Effects of antihistamines on 3,4-methylenedioxymethamphetamine-induced depletion of serotonin in rats." Synapse 33, no. 3 (September 1, 1999): 207–17. http://dx.doi.org/10.1002/(sici)1098-2396(19990901)33:3%3c207::aid-syn5%3e3.0.co;2-8.

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Yeh, S. Y., C. Dersch, R. Rothman, and J. L. Cadet. "Effects of antihistamines on 3,4-methylenedioxymethamphetamine-induced depletion of serotonin in rats." Synapse 33, no. 3 (September 1, 1999): 207–17. http://dx.doi.org/10.1002/(sici)1098-2396(19990901)33:3<207::aid-syn5>3.0.co;2-8.

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Tobback, Els, Olivier Desmet, Ignace Hanoulle, Liesbeth Delesie, Dirk Pevernagie, Dirk Vogelaers, and An Mariman. "Retrospective Analysis of Risk Factors for Periodic Limb Movements in a Large Cohort of Insomnia and Chronic Fatigue Patients." Pharmacopsychiatry 53, no. 02 (August 27, 2019): 71–77. http://dx.doi.org/10.1055/a-0991-0498.

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Abstract Introduction Although the pathophysiology of periodic limb movements in sleep (PLMS) is not well understood, there is increasing belief that management of PLMS can modulate humans’ general health. The aim of this study is to investigate the associations between risk factors including the use of antidepressants, hypnotics, and antihistamines as well as of caffeine, alcohol, and nicotine and the occurrence of PLMS and periodic limb movement disorder (PLMD). Methods Patients with either chronic fatigue or insomnia who underwent polysomnography as standardized clinical assessment were included in a retrospective study. Associations were calculated between substance use and sleep variables. Results Tricyclic antidepressants and serotonin and norepinephrine reuptake inhibitor (SNRI) are significantly associated with higher rates of PLMS. Additionally, SNRI is significantly positive associated with PLMD, as also seen for selective serotonin reuptake inhibitors (SSRI). The most frequently used SSRI escitalopram was significantly positively associated with PLMS and PLMD. A significantly negative association was found between paroxetine and PLMS. Benzodiazepines are negatively associated with PLMS and PLMD. Sedative antidepressants, antihistamines, and substance use are not associated with PLMS nor PLMD in this study. Discussion This retrospective study adds supportive evidence to the association of drug classes with PLMS and PLMD. These findings may impact on clinical management of patients with a combined anxiety or mood disorder in need for these drug classes on the one hand and a significant sleep architecture disturbance through PLMS, potentially contributing to daytime symptoms, on the other hand.
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Wauwe, J. P., and J. G. Goossens. "Arabinogalactan- and dextran-induced ear inflammation in mice: Differential inhibition by H1-antihistamines, 5-HT-serotonin antagonists and lipoxygenase blockers." Agents and Actions 28, no. 1-2 (August 1989): 78–82. http://dx.doi.org/10.1007/bf02022984.

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7

Lader, Malcolm. "Fluoxetine Efficacy vs Comparative Drugs: An Overview." British Journal of Psychiatry 153, S3 (September 1988): 51–58. http://dx.doi.org/10.1192/s0007125000297298.

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The tricyclic antidepressants (TCAs) were discovered accidentally by pharmaceutical chemists seeking first, better antihistamines and then antipsychotic agents. Careful clinical assessment revealed the antidepressant properties and suggested that the closer the patient resembled the classical textbook description of ‘endogenous’ depression, the more likely was an adequate clinical response to occur (Kuhn, 1958). However, it was quickly realised that the TCAs possess a plethora of side-effects, particularly sedation and symptoms related to their anticholinergic effects.Despite much research over the past 25 years, it is unclear how TCAs effect clinical improvement. The two main neurotransmitters involved in some way are noradrenaline (Schildkraut, 1965) and 5-hydroxytryptamine (5-HT; serotonin; Van Praag, 1977). It was proposed that TCAs acted by blocking the reuptake of one or other or both of these neurotransmitters, thereby increasing their concentration in the synaptic cleft. However, as well as these acute effects, chronic effects, such as a decrease in the number of central beta-adrenoceptors (‘down-regulation’) occur, and these are probably more relevant to the clinical action.
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8

Zamergrad, M. V., and S. V. Morozova. "Modern approaches to drug treatment for vestibular vertigo." Neurology, Neuropsychiatry, Psychosomatics 13, no. 1 (February 18, 2021): 101–6. http://dx.doi.org/10.14412/2074-2711-2021-1-101-106.

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In recent years, some progress has been achieved in elaborating the algorithms and standards for the treatment of many conditions accompanied by vertigo. The current possibilities of treating vestibular vertigo consist of a gradually expanding arsenal of symptomatic and pathogenetic drugs. Among the drugs used for the symptomatic treatment of vestibular vertigo, there are vestibular suppressants (antihistamines, benzodiazepines, and calcium antagonists) and antiemetics (dopamine antagonists and serotonin 5-HT3 receptor antagonists). The paper discusses the possibilities of using betahistine and vitamin D as pathogenetic agents for recurrent benign paroxysmal positional vertigo; diuretics, betahistine (including the new prolonged release formulation Betaserc® Long), glucocorticoids, and gentamicin for Meniere's disease; triptans, beta-blockers, tricyclic antidepressants, and anticonvulsants for vestibular migraine; glucocorticoids, antiviral agents, and drugs that accelerate vestibular compensation for acute unilateral peripheral vestibulopathy (vestibular neuritis and Ramsey Hunt syndrome).The emergence of new drugs, as well as the design of new dosage forms that enhance patient adherence to the prescribed treatment, can improve quality of life in patients suffering from diseases that have recently led to long-term disability or even incapacitation.
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9

Leslie, R. A., Y. Shah, M. Thejomayen, K. M. Murphy, and H. A. Robertson. "The neuropharmacology of emesis: the role of receptors in neuromodulation of nausea and vomiting." Canadian Journal of Physiology and Pharmacology 68, no. 2 (February 1, 1990): 279–88. http://dx.doi.org/10.1139/y90-042.

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The basic pharmacological mechanisms involved in mediating nausea and vomiting are still poorly understood. Several classes of drags have been identified that alleviate the symptoms of nausea and vomiting, either prophylactically or acutely. None of these is completely effective in all cases. They include antihistamines, dopamine antagonists, steroids, cannabinoids, benzodiazepines, serotonin antagonists, and anticholinergics. This paper examines the evidence that links each of these classes of drugs with the distribution of specific neurotransmitter receptor sites on which they may be acting. Studies on the central nervous system distribution of binding sites for one of these classes of drugs, the anticholinergics, are described. Binding sites for the muscarinic cholinergic radioligand [3H]quinuclidinyibenzilate occur in different concentrations throughout the dorsal vagal complex of the rabbit medulla oblongata. The distribution of such sites in this nonvomiting experimental animal is markedly different from that in the cat, an animal that has been used for many physiological and pharmacological studies of emesis. A previous study has suggested that muscarinic binding sites may occur presynaptically on vagal afferent terminals that synapse in the dorsal vagal complex of the cat; this appears not to be the case in the rabbit. Possible implications of these findings for the identification of the site of action of anticholinergic, antiemetic drags are discussed.Key words: neuromodulation, nausea, vomiting, receptors.
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10

Bartley, Jim. "Nasal Congestion and Hyperventilation Syndrome." American Journal of Rhinology 19, no. 6 (November 2005): 607–11. http://dx.doi.org/10.1177/194589240501900614.

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Background This article evaluates the prevalence of hyperventilation syndrome (HVS) in patients who continue to complain of ongoing nasal congestion, despite an apparently adequate surgical result and appropriate medical management. Methods Prospective case series of 14 patients from June 2002 to October 2003 was performed. Patients, who presented complaining of nasal congestion after previous nasal surgery and who appeared to have an adequate nasal airway with no evidence of nasal valve collapse, were evaluated for HVS. When appropriate, nasal steroids and oral antihistamines also had been tested without success. Three patients had end-tidal PCO2 levels measured and five patients underwent breathing reeducation. Results All patients had an elevated respiratory rate (>18 breaths/minute) with an upper thoracic breathing pattern. Twelve of the 14 patients complaining of nasal obstruction had an elevated Nijmegen score indicative of HVS. An average number of 2.5 procedures had been performed on each patient. End-tidal PCO2 levels were ≤35 mmHg in the three patients who had expired PCO2 levels measured. Breathing retraining was successful in correcting the nasal congestion in two of five patients. Conclusion HVS should be included in the differential diagnosis of patients presenting with nasal congestion, particularly after failed nasal surgery. One possible explanation is increased nasal resistance secondary to low arterial PCO2 levels. Another possible explanation is reduced alae nasae muscle activity secondary to the reduced activity of serotonin-containing raphe neurons. Additional surgery may not necessarily be the answer in HVS patients complaining of nasal congestion.
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Dissertations / Theses on the topic "Serotonin Antihistamines"

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Schooley, Elizabeth K. "The effects of an antiseritonergic drug and antihistamine in an experimental model of feline asthma." Diss., Columbia, Mo. : University of Missouri-Columbia, 2007. http://hdl.handle.net/10355/5033.

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Thesis (M.S.)--University of Missouri-Columbia, 2007.
The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. "May 2007" Includes bibliographical references.
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Conference papers on the topic "Serotonin Antihistamines"

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Pillgram-Larsen, J., T. E. Ruud, J. O. Stadaas, and A. O. Aasen. "MULTITHERAPY PRETREATMENT IMPROVES HEMODYNAMIC FUNCTION IN EXPERIMENTAL ENDOTOXEMIA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644892.

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To evaluate the cardiopulmonary response to a newregimen of therapy in endotoxemia, ten pigs were infused with endotoxin 0.01 mg/kg over three hours. Five animals (treatment group) received therapy starting 30 min prior to endotoxin infusion consisting of repeated doses of protease inhibitor concentrates (C1esterase inhibitor 2000 IU, antithrombin III 500 IU,aprotinin 2 mill KIU), methylprednisolone 100 mg/kg, antihistamine(promethazin 1 mg/kg), a serotonin antagonist (ketanserine 2 mg/kg) and an opiate antagonist (naloxone 0.06 mg/kg). Five animals were untreated.Eight animals (control group) were anaesthetized and observed without endotoxin or treatment. The observation time was five hours. Two untreated animals receiving endotoxin died. Endotoxin caused a decrease in cardiac function with decreased left ventricular stroke work (LVSW). Endotoxin resulted in a marked increase in pulmonary vascular resistance (PVR) and oxygenation was impaired. With multiherapy cardiac output increased. Systemic vascular resistence was decreased in the treatment group while it increased steadily in the untreated group. LVSW was significantlybetter maintained in the treated animals. Pulmonary vascular resistence was unaltered in the treatment group. Pulmonary gas exchange was not different between the endotoxin infused groups. Endotoxin infusion caused no metabolic changes in this short time modelas oxygen consumption was not different between the three groups. Overall cardiopulmonary function was improved in treated animals compared to both untreated endotoxin infused animals and controls as mixed venous oxygen saturation was higher in the treatment group. Multitherapy has a protective effect on cardiopulmonary functions in experimental endotoxemia.
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Journal articles
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