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Histamine release from sensitized

Histamine release from pig lung occurs in response to extracts from cotton pericarp, seed, leaf, root and bract (112). Extracts of sisal release histamine from both pig and human lung, but the reactivity is less than cotton dust extracts. The use of chopped lung for histamine assay is not always reliable, however, nor is it sufficiently sensitive. [Pg.155]

Insulin allergy, an immediate type hypersensitivity, is a rare condition in which local or systemic urticaria results from histamine release from tissue mast cells sensitized by anti-insulin IgE antibodies. In severe cases, anaphylaxis results. Because sensitivity is often to noninsulin protein contaminants, the human and analog insulins have markedly reduced the incidence of insulin allergy, especially local reactions. [Pg.939]

Fig. 1.1 Interaction between allergen and adenosine receptor agonists with respect to histamine release from guinea-pig chopped lung (left) or bronchoconstriction in the guinea pig in vivo (right). Tissues and animals were passively sensitized to ovalbumin. In the histamine release assay, a threshold response to allergen is augmented concentration-dependently by NECA. In the whole animal, a single intravenous injection of APNEA markedly enhances the bronchoconstrictor response to allergen (J.R. Fozard and H.J. Pfannkuche, unpublished observations 1994)... Fig. 1.1 Interaction between allergen and adenosine receptor agonists with respect to histamine release from guinea-pig chopped lung (left) or bronchoconstriction in the guinea pig in vivo (right). Tissues and animals were passively sensitized to ovalbumin. In the histamine release assay, a threshold response to allergen is augmented concentration-dependently by NECA. In the whole animal, a single intravenous injection of APNEA markedly enhances the bronchoconstrictor response to allergen (J.R. Fozard and H.J. Pfannkuche, unpublished observations 1994)...
Q3 A type 1 hypersensitivity reaction is responsible for the development of the allergy. The symptoms are due to the effects of mast cell degranulation with the release of histamine. Mast cells are located in the nasal passages and the nasal mucosa is sensitive to the effects of histamine released from these cells, leading to inflammation of the mucous membranes of the nose. The inflammation is associated with oedema and swelling, vasodilation and an increase in the secretion of mucus. The mucous membrane of other sections of the respiratory tract (accessory sinuses, nasopharynx, and upper and lower respiratory tract) will also be affected by the allergic reaction. [Pg.204]

The mechanism by which cyclooxygenase inhibition produces bronchospasm in susceptible individuals is unknown. Arachidonic acid metabolism through the 5-lipoxygenase pathway may lead to the excess production of leukotrienes C4 and D4. Leukotrienes C4, D4, and E4 produce bronchospasm and promote histamine release from mast cells, whereas the administration of leukotriene receptor antagonists and 5-lipoxygenase inhibitors ablate the pulmonary and nonpuhnonary responses to aspirin in aspirin-sensitive asthmatics. The precise mechanism by which augmented leukotriene production occurs is unknown, and available hypotheses do not explain why only a small number of asthmatic patients react to aspirin and NSAIDs. [Pg.579]

A number of new orally active MRI s have been described. The oxamic acid (22) (PRH-836-EA) has an ED of 0.6 mg/kg p.o. in the rat PCA assayJ °The quinazoline carboxylate V23) was orally active (ED-q = 0.05 mg/kg) against anaphylactic bronchospasm in passively sensitized rats and inhibited the antigen-induced histamine release from passively... [Pg.97]

Bassi et al. (1976) have since demonstrated human IgE antibodies to rifampicin by means of histamine release from passively sensitized peritoneal mast cells. The sera were obtained from patients showing side effects to rifampicin therapy. These results seem to provide further evidence for an immunologic origin of the adverse reactions to rifampicin. [Pg.504]

Strongly positive skin tests and histamine release from basophils confirmed a sensitivity to pitressin in a patient who had anaphylactic shock following administration of this hormone (Lawrence et al. 1972). The presence of reaginic-like antibodies to pituitary protein and to lysine vasopressin has also been confirmed by PK tests (OsvATH et al. 1970). [Pg.705]

Whigham, L.D., Cook, E.B., Stahl, J.L., Saban, R., BjorUng, D.E., Pariza, M.W., and Cook, M.E. (2001) CLA Reduces Antigen-Induced Histamine and PGE(2) Release from Sensitized Guinea Pig Tracheae, Am. J. Physiol. 280, R908-R912. [Pg.264]

Katsu, T Kanamitsu, M Hirota, T. etal. (1986) In situ detection of histamine released from mast-cells by using a histamine-sensitive membrane-electrode. Chem. Pharm. Bull., 34, 3968-3970. [Pg.204]

Katsu, T. and Hirodo, H. (1999) Determination of histamine release from mast cells using a histamine-sensitive membrane electrode. Anal. Chim. Acta, 396, 189-193. [Pg.204]


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