The Experts below are selected from a list of 225 Experts worldwide ranked by ideXlab platform
Miho Shimada - One of the best experts on this subject based on the ideXlab platform.
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Cetirizine a histamine H1 receptor Antagonist improves viral myocarditis
Journal of Inflammation, 2010Co-Authors: Akira Matsumori, Kanjo Yamamoto, Miho ShimadaAbstract:Background We showed that mast cells played a critical role in the progression of heart failure induced by pressure overload and viral myocarditis in mice. In this study, we investigated the effect of cetirizine, a selective H1 receptor Antagonist, on experimental viral myocarditis induced by encephalomyocarditis (EMC) virus. Methods Four-week-old inbred male DBA/2 mice were inoculated intraperitoneally with 10 plaque-forming units (pfu) of the EMC virus. Cetirizine was administered orally at a dose of 1 or 10 mg/kg per day for the survival study, and 1 mg/kg for the histologic and gene expression studies, beginning on the day of viral inoculation. Results Cetirizine improved survival dose dependently. Heart weight to body weight ratio was significantly decreased in mice treated with cetirizine. The area of myocardial necrosis was significantly smaller in the hearts of mice treated with cetirizine compared with controls. Gene expressions of tumor necrosis factor, interleukin 6, and metalloproteinase 2 were significantly suppressed in the hearts of mice treated with cetirizine. Conclusion These results suggest that cetirizine exerts its beneficial effects on viral myocarditis by suppressing expression of pro-inflammatory cytokines, genes related to cardiac remodeling in the hearts of mice.
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Cetirizine a histamine H1 receptor Antagonist improves viral myocarditis
Journal of inflammation (London England), 2010Co-Authors: Akira Matsumori, Kanjo Yamamoto, Miho ShimadaAbstract:Background We showed that mast cells played a critical role in the progression of heart failure induced by pressure overload and viral myocarditis in mice. In this study, we investigated the effect of cetirizine, a selective H1 receptor Antagonist, on experimental viral myocarditis induced by encephalomyocarditis (EMC) virus.
Akira Matsumori - One of the best experts on this subject based on the ideXlab platform.
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Cetirizine a histamine H1 receptor Antagonist improves viral myocarditis
Journal of Inflammation, 2010Co-Authors: Akira Matsumori, Kanjo Yamamoto, Miho ShimadaAbstract:Background We showed that mast cells played a critical role in the progression of heart failure induced by pressure overload and viral myocarditis in mice. In this study, we investigated the effect of cetirizine, a selective H1 receptor Antagonist, on experimental viral myocarditis induced by encephalomyocarditis (EMC) virus. Methods Four-week-old inbred male DBA/2 mice were inoculated intraperitoneally with 10 plaque-forming units (pfu) of the EMC virus. Cetirizine was administered orally at a dose of 1 or 10 mg/kg per day for the survival study, and 1 mg/kg for the histologic and gene expression studies, beginning on the day of viral inoculation. Results Cetirizine improved survival dose dependently. Heart weight to body weight ratio was significantly decreased in mice treated with cetirizine. The area of myocardial necrosis was significantly smaller in the hearts of mice treated with cetirizine compared with controls. Gene expressions of tumor necrosis factor, interleukin 6, and metalloproteinase 2 were significantly suppressed in the hearts of mice treated with cetirizine. Conclusion These results suggest that cetirizine exerts its beneficial effects on viral myocarditis by suppressing expression of pro-inflammatory cytokines, genes related to cardiac remodeling in the hearts of mice.
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Cetirizine a histamine H1 receptor Antagonist improves viral myocarditis
Journal of inflammation (London England), 2010Co-Authors: Akira Matsumori, Kanjo Yamamoto, Miho ShimadaAbstract:Background We showed that mast cells played a critical role in the progression of heart failure induced by pressure overload and viral myocarditis in mice. In this study, we investigated the effect of cetirizine, a selective H1 receptor Antagonist, on experimental viral myocarditis induced by encephalomyocarditis (EMC) virus.
Kanjo Yamamoto - One of the best experts on this subject based on the ideXlab platform.
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Cetirizine a histamine H1 receptor Antagonist improves viral myocarditis
Journal of Inflammation, 2010Co-Authors: Akira Matsumori, Kanjo Yamamoto, Miho ShimadaAbstract:Background We showed that mast cells played a critical role in the progression of heart failure induced by pressure overload and viral myocarditis in mice. In this study, we investigated the effect of cetirizine, a selective H1 receptor Antagonist, on experimental viral myocarditis induced by encephalomyocarditis (EMC) virus. Methods Four-week-old inbred male DBA/2 mice were inoculated intraperitoneally with 10 plaque-forming units (pfu) of the EMC virus. Cetirizine was administered orally at a dose of 1 or 10 mg/kg per day for the survival study, and 1 mg/kg for the histologic and gene expression studies, beginning on the day of viral inoculation. Results Cetirizine improved survival dose dependently. Heart weight to body weight ratio was significantly decreased in mice treated with cetirizine. The area of myocardial necrosis was significantly smaller in the hearts of mice treated with cetirizine compared with controls. Gene expressions of tumor necrosis factor, interleukin 6, and metalloproteinase 2 were significantly suppressed in the hearts of mice treated with cetirizine. Conclusion These results suggest that cetirizine exerts its beneficial effects on viral myocarditis by suppressing expression of pro-inflammatory cytokines, genes related to cardiac remodeling in the hearts of mice.
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Cetirizine a histamine H1 receptor Antagonist improves viral myocarditis
Journal of inflammation (London England), 2010Co-Authors: Akira Matsumori, Kanjo Yamamoto, Miho ShimadaAbstract:Background We showed that mast cells played a critical role in the progression of heart failure induced by pressure overload and viral myocarditis in mice. In this study, we investigated the effect of cetirizine, a selective H1 receptor Antagonist, on experimental viral myocarditis induced by encephalomyocarditis (EMC) virus.
F. E. R. Simons - One of the best experts on this subject based on the ideXlab platform.
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Is antihistamine (H1‐receptor Antagonist) therapy useful in clinical asthma?
Clinical & Experimental Allergy, 1999Co-Authors: F. E. R. SimonsAbstract:Airway hyperresponsiveness to histamine is a hallmark of asthma, and histamine inhalation reproduces asthma symptoms. Plasma histamine concentrations are elevated during the early and late responses to inhaled allergens, and may also increase during spontaneous acute asthma episodes. Ordinary doses of currently available antihistamines (H1-Receptor Antagonists) have minimal bronchodilator and bronchoprotective activity. In severe persistent asthma, H1 Antagonists have no significant clinical effect. In moderate persistent asthma, clinical benefits of H1 Antagonists are apparent, but may not be worth the potential risks of the higher-than-usual doses required. When mild seasonal asthma and allergic rhinitis coexist, however, relief of rhinitis symptoms with H1 Antagonists administered in ordinary dose is associated with significant improvement in asthma symptoms.
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Evolution of H1-Receptor Antagonist treatment.
Annals of allergy, 1993Co-Authors: F. E. R. SimonsAbstract:The introduction of relatively nonsedating H 1 -receptor Antagonists ushered in a new era in the symptomatic treatment of allergic disorders. Unlike first-generation H 1 -receptor Antagonists, the second-generation compounds (such as astemizole, cetirizine, loratadine, and terfenadine) do not cross the blood-brain barrier readily and are thus comparatively free of central nervous system effects. The pharmacokinetic and pharmacodynamic profiles vary considerably by agent, but most of the second-generation drugs are suitable for once-daily dosing
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Evolution of H1-Receptor Antagonist treatment.
Annals of allergy, 1993Co-Authors: F. E. R. SimonsAbstract:The introduction of relatively nonsedating H1-Receptor Antagonists ushered in a new era in the symptomatic treatment of allergic disorders. Unlike first-generation H1-Receptor Antagonists, the second-generation compounds (such as astemizole, cetirizine, loratadine, and terfenadine) do not cross the blood-brain barrier readily and are thus comparatively free of central nervous system effects. The pharmacokinetic and pharmacodynamic profiles vary considerably by agent, but most of the second-generation drugs are suitable for once-daily dosing. Efficacy of the H1 Antagonists is maintained during chronic therapy. The second-generation H1-Receptor Antagonists are appropriate for use as first-line treatment of allergic rhinoconjunctivitis and urticaria. These agents also have a modest, direct beneficial effect in patients with chronic asthma. The role of the newer H1-Receptor Antagonists in the treatment of atopic dermatitis, upper respiratory tract infections, and otitis media remains undefined. Recently, the gene encoding the histamine H1 receptor was cloned from bovine adrenal medullae. Emerging evidence suggests that more than one subtype of H1 receptor may exist. It is hoped these advances will pave the way for further improvements in H1-Antagonist therapy.
Lawrence M Du Buske - One of the best experts on this subject based on the ideXlab platform.
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clinical comparison of histamine h1 receptor Antagonist drugs
The Journal of Allergy and Clinical Immunology, 1996Co-Authors: Lawrence M Du BuskeAbstract:Nearly 40 million Americans have symptoms of upper respiratory allergies, making antihistamines among the most frequently used pharmacologic agents. Although there are mediators of allergic symptoms in addition to histamine, therapy for allergic rhinitis and urticaria has focused upon the use of antihistamines. The classic histamine H1-Receptor Antagonists, however, are not selective for the H1 site and produce a variety of dopaminergic, serotonergic, and cholinergic responses leading to considerable adverse effects in the central nervous system consequent to both their pharmacologic nonselectivity and their ability to penetrate the blood-brain barrier readily. The second-generation antihistamines were a major advance in the therapy of allergic rhinitis, because they do not penetrate the blood-brain barrier as rapidly and are also designed for greater specificity at H1-Receptor. Given their greater selectivity for the H1-Receptor, they cause fewer undesirable central nervous system actions, whereas their efficacy is similar to that of the classic antihistamines used in the treatment of allergic rhinitis. Selecting among these antihistamines for the treatment of allergic rhinitis has focused on their pharmacokinetics and adverse effect profiles. The potential cardiotoxic effects of some antihistamines when their metabolism is inhibited requires caution in prescribing these agents. The antiallergic and antiasthmatic effects of several newer antihistamines are being explored. For the clinician, making the therapeutic decision among H1-Receptor Antagonists requires a comprehensive knowledge of their diverse effects.
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Clinical comparison of histamine H1–receptor Antagonist drugs
Journal of Allergy and Clinical Immunology, 1996Co-Authors: Lawrence M Du BuskeAbstract:Nearly 40 million Americans have symptoms of upper respiratory allergies, making antihistamines among the most frequently used pharmacologic agents. Although there are mediators of allergic symptoms in addition to histamine, therapy for allergic rhinitis and urticaria has focused upon the use of antihistamines. The classic histamine H1-Receptor Antagonists, however, are not selective for the H1 site and produce a variety of dopaminergic, serotonergic, and cholinergic responses leading to considerable adverse effects in the central nervous system consequent to both their pharmacologic nonselectivity and their ability to penetrate the blood-brain barrier readily. The second-generation antihistamines were a major advance in the therapy of allergic rhinitis, because they do not penetrate the blood-brain barrier as rapidly and are also designed for greater specificity at H1-Receptor. Given their greater selectivity for the H1-Receptor, they cause fewer undesirable central nervous system actions, whereas their efficacy is similar to that of the classic antihistamines used in the treatment of allergic rhinitis. Selecting among these antihistamines for the treatment of allergic rhinitis has focused on their pharmacokinetics and adverse effect profiles. The potential cardiotoxic effects of some antihistamines when their metabolism is inhibited requires caution in prescribing these agents. The antiallergic and antiasthmatic effects of several newer antihistamines are being explored. For the clinician, making the therapeutic decision among H1-Receptor Antagonists requires a comprehensive knowledge of their diverse effects.