The role of H2-receptors in bronchial reactivity in atopic asthma

Hofman, J; Michalska, I; Rutkowski, Ryszard; Chyrek-Borowska, S

doi:10.1007/bf02142590

Cited by 3 publications

(1 citation statement)

References 8 publications

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“…(4,31) Moreover, some findings seem to suggest that the presumptive protective effect of ranitidine can be nullified, and its use may become even dangerous in patients who develop anaphylaxis because of the increased risk of heart block or bronchial hyperreactivity. (32,33) …”

Section: Discussionmentioning

confidence: 98%

Hypersensitivity reaction to ranitidine: Description of a case and review of the literature

Foti

Cassano

Panebianco

et al. 2009

Immunopharmacology and Immunotoxicology

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Ranitidine is an H2-receptor antagonist which is usually well tolerated. Hypersensitivity reactions to ranitidine, as well as other H2 antihistamines, have been rarely described. We report the case of a 47-year-old woman who developed an anaphylactic reaction to ranitidine used as intravenous premedication before anesthesia induction. The patient's history revealed that previous use of oral ranitidine for a peptic ulcer disease did not cause any adverse reaction. Intradermal test with ranitidine at a dilution of 1:100 gave an intense positive reaction. The protective role of H2-receptor antagonists as premedication is still unclear and should be carefully reconsidered on the basis of the available controversial evidence and the possible risk of hypersensitivity reactions.

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Section: Discussionmentioning

confidence: 98%

Hypersensitivity reaction to ranitidine: Description of a case and review of the literature

Foti

Cassano

Panebianco

et al. 2009

Immunopharmacology and Immunotoxicology

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Comparison of the effects of cimetidine and ranitidine in histamine provocation tests in atopic asthma

1989

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The effects of cimetidine and ranitidine on the bronchial reactivity in the group of 10 patients with atopic bronchial asthma are presented. The patients received 800 mg of cimetidine daily for 6 days and, after a three-day interval, 300 mg of ranitidine daily for a further 6 days. Bronchial reactivity to histamine was determined before the administration of each drug and on the third and sixth days of each course of treatment. A comparison of the effect of cimetidine and ranitidine on the bronchial reactivity of the same patients revealed that after 3 days' exposure to each of the two drugs, cimetidine enhanced bronchial reactivity to a statistically (p less than 0.05) greater extent than ranitidine. Bronchial reactivity was found to increase significantly after 6 days of treatment with each of the drugs but no statistically significant differences were noted on comparing the effect of these drugs. The results seem to indicate that H2 receptor antagonists may cause bronchoconstriction in some patients with bronchial asthma. The blocking effect depends on the type of the drug used and is connected with the chemical structure of the compounds.

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The Response of a Human Bronchial Epithelial Cell Line to Histamine: Intracellular Calcium Changes and Extracellular Release of Inflammatory Mediators

Noah

Paradiso²,

Madden³

et al. 1991

Am J Respir Cell Mol Biol

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Epithelial cells are likely to modulate inflammation and tissue repair in the airways, but the factors responsible for these processes remain unclear. Because human airway epithelia are infrequently available for in vitro studies, transformed epithelial cell lines are of interest as models. We therefore investigated the response of an SV-40/adenovirus-transformed human bronchial epithelial cell line (BEAS-2B) to histamine, a mediator with relevance for airway diseases. The intracellular calcium response to histamine (10(-4) M) was measured, using Fura-2 and microspectrofluorimetry. Histamine induced a transient increase in intracellular calcium that originated from intracellular sources; this effect was inhibited by the H1 receptor antagonist diphenhydramine, suggesting that BEAS cells retain functioning histamine receptors. BEAS cells were grown to confluence on microporous, collagen-coated filters, allowing measurement of vectorial release of soluble mediators. Monolayers exposed to histamine for 30 min released interleukin-6 and fibronectin in the apical direction, in a dose-dependent manner. Little eicosanoid production was induced by histamine, either in the apical or the basolateral direction, although BEAS cells constitutively produced small amounts of prostaglandin E2 and 15-HETE. However, these cells formed large amounts of eicosanoids in response to ozone exposure as a positive control. Comparison of our data with published reports for human airway epithelia in primary culture suggests that the BEAS cell line is, in a number of respects, a relevant model for the study of airway epithelial responses to a variety of stimuli.

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The role of H2-receptors in bronchial reactivity in atopic asthma

Cited by 3 publications

References 8 publications

Hypersensitivity reaction to ranitidine: Description of a case and review of the literature

Hypersensitivity reaction to ranitidine: Description of a case and review of the literature

Comparison of the effects of cimetidine and ranitidine in histamine provocation tests in atopic asthma

The Response of a Human Bronchial Epithelial Cell Line to Histamine: Intracellular Calcium Changes and Extracellular Release of Inflammatory Mediators

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