Possible role of histamine (H1- and H2-) receptors in the regulation of meningeal blood flow. HLA-DR and ICAM-1 expression and modulation in epithelial cells from nasal polyps. Effects of second generation of histamine H1 antagonists, cetirizine and ebastine, on the antitussive and rewarding effects of dihydrocodeine in mice. Rx drugs

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Br J Pharmacol. 2002 Nov;137(6):874-80.
Possible role of histamine (H1- and H2-) receptors in the regulation of meningeal blood flow.

Dux M, Schwenger N, Messlinger K.

Department of Physiology, University of Szeged, Faculty of Medicine, Dom ter 10, 6720 Szeged, Hungary.

1. Vasodilatation in the dura mater has been suggested to play an important role in the pathophysiology of vascular headaches. Histamine may contribute to these vascular changes. The aim of the present study was to examine the role of different histamine receptors in histamine-induced meningeal hyperperfusion using laser Doppler flowmetry. 2. The blood flow in the medial meningeal artery was monitored in the exposed parietal dura mater encephali of barbiturate anaesthetized rats. Local application of histamine (10(-5) and 10(-4) M) onto the dura caused increases in flow to 114.2+/-9.6 and 135.1+/-19.1%, respectively, of the basal flow. 3. Flow increases induced by topical application of histamine (10(-4) M) were reduced by local pretreatment with the H(2)-receptor antagonist cimetidine (0.4 and 4 mM) to 63.4+/-17 and 37.8+/-18.8%, respectively. Systemic pre-administration of cimetidine (5 mg kg(-1) i.v.) did not change histamine-induced flow increases. 4. Local pretreatment with the H(1)-receptor antagonist cetirizine (2 micro M) further increased the flow evoked by topical histamine administration (10(-4) M) to 123.5+/-14.7% of the histamine control. 5. Increases in blood flow induced by i.v. administration of histamine (10 micro g kg(-1)) were reduced by i.v. pre-injection of cetirizine (50 micro g kg(-1)) to 31.9+/-9% but not by i.v. cimetidine (5 mg kg(-1)). 6. We conclude that histamine-induced relaxation of dural arterial vessels is mediated by H(2)-receptors, most likely located on vascular smooth muscle cells, and by endothelial H(1)-receptors. In addition, H(1)-receptors on smooth muscle cells may mediate vasoconstriction.

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Laryngoscope. 2002 Nov;112(11):2067-75.
HLA-DR and ICAM-1 expression and modulation in epithelial cells from nasal polyps.

Papon JF, Coste A, Gendron MC, Cordonnier C, Wingerstmann L, Peynegre R, Escudier E.

Institut National de la Sante et de la Recherche Medicale, Unite U492, Faculte de Medecine, Paris XII, Creteil, France.

OBJECTIVE/HYPOTHESIS: Through human leukocyte antigen-DR (HLA-DR) and intercellular adhesion molecule-1 (ICAM-1) expression, nasal epithelial cells could actively participate in the chronic inflammation and eosinophil infiltration observed in nasal polyps. The objective of the study was to evaluate HLA-DR and ICAM-1 expression in polyp epithelium and in a culture model of polyp epithelial cells allowing ciliated and secretory differentiation. STUDY DESIGN: Prospective non-randomized controlled in vitro study. METHODS: The in vitro HLA-DR and ICAM-1 expression was studied under basal conditions or after exposure to interferon-gamma, transforming growth factor-beta1, lipopolysaccharide, dexamethasone, or cetirizine. HLA-DR and ICAM-1 expression was investigated in situ by immunohistochemical staining of polyps and in vitro by immunofluorescent staining of cell cultures. HLA-DR and ICAM-1 were localized in cultured cells by confocal microscopy. Cultured cells expressing HLA-DR and ICAM-1 were quantified by flow cytometry. RESULTS: Both HLA-DR and ICAM-1 showed significant immunostaining of nasal polyp epithelium. In nasal polyp epithelial cell cultures, less than 5% of cells were positive for HLA-DR whereas 40% were positive for ICAM-1 at day 3. In vitro, HLA-DR was mainly located in the cytoplasm and ICAM-1 predominated on the apicolateral cytoplasmic membrane. Comparison of in situ and in vitro results showed that well-differentiated and poorly differentiated cells predominantly expressed HLA-DR and ICAM-1, respectively. Interferon-gamma significantly increased HLA-DR and ICAM-1 expression, whereas transforming growth factor-beta1 significantly decreased HLA-DR expression and lipopolysaccharide significantly increased ICAM-1 expression. CONCLUSION: HLA-DR and ICAM-1 epithelial expression in nasal polyps in situ and in vitro and their in vitro modulation reinforce the active role of epithelial cells in chronic inflammatory diseases of the upper airways.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12439183&dopt=Abstract

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Psychopharmacology (Berl). 2003 Mar;166(2):176-80. Epub 2003 Jan 21.
Effects of second generation of histamine H1 antagonists, cetirizine and ebastine, on the antitussive and rewarding effects of dihydrocodeine in mice.

Kamei J, Morita K, Miyata S, Onodera K.

Department of Pathophysiology & Therapeutics, School of Pharmacy and Pharmaceutical Sciences, Hoshi University, Shinagawa-ku, 142-8501, Tokyo, Japan.

RATIONALE: Little information is available about the interaction between dihydrocodeine and second-generation antihistamine drugs such as cetirizine and ebastine, with particular reference to the rewarding effect of dihydrocodeine. OBJECTIVE: The effects of second generation histamine H(1) antagonists, such as cetirizine and ebastine on the antitussive and rewarding effect of dihydrocodeine were examined in mice. METHODS: Mice were exposed to a nebulized solution of capsaicin (30 micromol/l) under conscious and identical conditions, using a body plethysmograph. The coughs produced during a 3-min exposure period were counted. Effects of H(1) antagonists on the reinforcing effect of dihydrocodeine were assessed by using the conditioned place preference procedure in mice. RESULTS: The antitussive effect of dihydrocodeine was enhanced by the simultaneous administration of either cetirizine or ebastine. There was no statistical difference between the ED(50) of dihydrocodeine in combination with ebastine and that of dihydrocodeine in combination with cetirizine. Concurrent dosing of dihydrocodeine and ebastine produced a significant place preference. This behavioral potentiation was antagonized by SCH23390, a dopamine D(1) antagonist. Moreover, ebastine enhanced the central dopamine turnover ratio, but cetirizine could not, in this study. CONCLUSION: Taken together, the potentiation of place preference of dihydrocodeine with ebastine may be due, at least in part, to stimulation of the central dopaminergic system via D(1) receptors. However, combination of dihydrocodeine with cetirizine does not potentiate place preference at all, nor does it potentiate the central dopaminergic system. Thus, it is likely that cetirizine may be a useful constituent in opioid-containing, antitussive preparations that would not potentiate the development of psychological dependence.

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