MEDIATORS OF IgE-INDUCED ANAPHYLAXIS: AN IN VITRO STUDY OF MEDIATORS CAUSING CONTRACTION OF RABBIT PULMONARY ARTERY

Persistent Link:
http://hdl.handle.net/10150/291622
Title:
MEDIATORS OF IgE-INDUCED ANAPHYLAXIS: AN IN VITRO STUDY OF MEDIATORS CAUSING CONTRACTION OF RABBIT PULMONARY ARTERY
Author:
Wiese, Anne Carroll Gordon, 1956-
Issue Date:
1987
Publisher:
The University of Arizona.
Rights:
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
Abstract:
Rabbits were immunized such that antibodies of the IgE class were preferentially produced. Normal rabbit pulmonary artery sections were challenged with supernatant from antigen-treated sensitized blood cells in the presence of antagonists. The hypothesis is that mediators capable of contracting pulmonary arteries are released from blood cells when blood cells are challenged with antigen. Possible mediators are histamine, serotonin, indomethacin and LTD4. Chlorpheniramine (2.6 x 10⁻⁵M) with methysergide (1 x 10⁻⁵ produced a one-hundred-twenty-fold inhibition of contraction. Chlorpheniramine with FPL-55712 (1 x 10⁻⁵M) did not significantly alter the response seen with chlorpheniramine alone. When supernatant obtained from sensitized blood cells pretreated with 1 x 10⁻⁵ indomethacin was used to challenge muscle rings in the presence of chlorpheniramine the response was also not significantly different from response seen with chlorpheniramine alone. Histamine contracted pulmonary artery. Chlorpheniramine (2.6 x 10⁻⁵ inhibited the response six-hundred-fold. Serotonin also contracted pulmonary artery. Methysergide (10⁻⁵M) blocked the response seven-hundred-fold.
Type:
text; Thesis-Reproduction (electronic)
Keywords:
Antigens.; Anaphylaxis.; Immunoglobulin E.
Degree Name:
M.S.
Degree Level:
masters
Degree Program:
Graduate College; Pharmacology and Toxicology
Degree Grantor:
University of Arizona
Advisor:
Halonen, Marilyn J.

Full metadata record

DC FieldValue Language
dc.language.isoen_USen_US
dc.titleMEDIATORS OF IgE-INDUCED ANAPHYLAXIS: AN IN VITRO STUDY OF MEDIATORS CAUSING CONTRACTION OF RABBIT PULMONARY ARTERYen_US
dc.creatorWiese, Anne Carroll Gordon, 1956-en_US
dc.contributor.authorWiese, Anne Carroll Gordon, 1956-en_US
dc.date.issued1987en_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.description.abstractRabbits were immunized such that antibodies of the IgE class were preferentially produced. Normal rabbit pulmonary artery sections were challenged with supernatant from antigen-treated sensitized blood cells in the presence of antagonists. The hypothesis is that mediators capable of contracting pulmonary arteries are released from blood cells when blood cells are challenged with antigen. Possible mediators are histamine, serotonin, indomethacin and LTD4. Chlorpheniramine (2.6 x 10⁻⁵M) with methysergide (1 x 10⁻⁵ produced a one-hundred-twenty-fold inhibition of contraction. Chlorpheniramine with FPL-55712 (1 x 10⁻⁵M) did not significantly alter the response seen with chlorpheniramine alone. When supernatant obtained from sensitized blood cells pretreated with 1 x 10⁻⁵ indomethacin was used to challenge muscle rings in the presence of chlorpheniramine the response was also not significantly different from response seen with chlorpheniramine alone. Histamine contracted pulmonary artery. Chlorpheniramine (2.6 x 10⁻⁵ inhibited the response six-hundred-fold. Serotonin also contracted pulmonary artery. Methysergide (10⁻⁵M) blocked the response seven-hundred-fold.en_US
dc.typetexten_US
dc.typeThesis-Reproduction (electronic)en_US
dc.subjectAntigens.en_US
dc.subjectAnaphylaxis.en_US
dc.subjectImmunoglobulin E.en_US
thesis.degree.nameM.S.en_US
thesis.degree.levelmastersen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.disciplinePharmacology and Toxicologyen_US
thesis.degree.grantorUniversity of Arizonaen_US
dc.contributor.advisorHalonen, Marilyn J.en_US
dc.identifier.proquest1331429en_US
dc.identifier.oclc17576188en_US
dc.identifier.bibrecord.b16337256en_US
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