Drugs online research references
Allergol Immunopathol (Madr). 1992 Sep-Oct;20(5):207-10.
Studies of nonsedative antihistamines. II. Assessment of its antihistaminic potency.
Aparicio S, Granel C, Randazzo L, Valencia M, Olive Perez A.
Hospital de la Santa Creu i Sant Pau, Unitat d'Al.lergia, Barcelona.
An analysis is made of the effectiveness of terfenadine at dosages of 60 and 120 mg, of cetirizine at a dose of 10 mg, and of loratadine and ebastine at a dose of 10 mg in inhibiting the papule induced by 20 mcg of intradermal histamine. Although all produced significant inhibition, cetirizine and terfenadine 120 mg showed a significantly greater inhibition coefficient than loratadine.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1363340&dopt=Abstract
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Br J Dermatol. 1992 Aug;127(2):85-90.
Further studies on the actions of endothelin-1 on blood flow in human skin.
Bunker CB, Coulson ML, Hayes NA, Dowd PM, Foreman JC.
Department of Dermatology, University College and Middlesex School of Medicine, University College London, U.K.
When injected into human skin, endothelin-1 produces intense vasoconstriction localized to the site of the injection, but this area of vasoconstriction is surrounded by vasodilatation which spreads several centimetres from the injection site. The vasodilatation induced by intradermal injection of endothelin-1 (63 pmol) into human skin is prevented by local anaesthetic. Pretreatment of human skin with capsaicin also inhibits this response. Pretreatment of subjects with the selective histamine H1-receptor antagonist cetirizine, 10 mg orally 4 h before intradermal injections, inhibited vasodilatation caused by the intradermal injection of histamine (750 pmol), endothelin-1 (63 pmol), and carbachol (750 pmol). Endothelin-1 (0.3-10 microM) and carbachol (1-30 microM) failed to induce histamine release from rat peritoneal mast cells. We conclude that the vasodilatation caused by intradermal injection of endothelin-1 into human skin is neurogenic and is probably mediated by neuropeptide-containing primary afferent neurones. Because neither carbachol nor endothelin-1 cause histamine release from mast cells, our data suggest that histamine release from mast cells at the effector end of the axon reflex is responsible for the carbachol- and endothelin-induced vasodilatation in human skin.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1382539&dopt=Abstract
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gsk.com
Recent in vitro studies have suggested that P-glycoprotein (Pgp) and passive membrane permeability may influence the brain concentrations of non-sedating (second-generation) antihistamines. The purpose of this study was to determine the importance of Pgp-mediated efflux on the in vivo brain distribution of the non-sedating antihistamine cetirizine (Zyrtec), and the structurally related sedating (first-generation) antihistamine hydroxyzine (Atarax). In vitro MDR1-MDCKII monolayer efflux assays demonstrated that cetirizine was a Pgp substrate (B-->A/A-->B + GF120918 ratio = 5.47) with low/moderate passive permeability (PappB-->A = 56.5 nm/s). In vivo, the cetirizine brain-to-free plasma concentration ratios (0.367 to 4.30) were 2.3- to 8.7-fold higher in Pgp-deficient mice compared with wild-type mice. In contrast, hydroxyzine was not a Pgp substrate in vitro (B-->A/A-->B ratio = 0.86), had high passive permeability (PappB-->A + GF120918 = 296 nm/s), and had brain-to-free plasma concentration ratios >73 in both Pgp-deficient and wild-type mice. These studies demonstrate that Pgp-mediated efflux and passive permeability contribute to the low cetirizine brain concentrations in mice and that these properties account for the differences in the sedation side-effect profiles of cetirizine and hydroxyzine. Copyright 2003 Wiley-Liss, Inc. and the American Pharmacists Association
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14502547&dopt=Abstract [PubMed - in process]
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