The role of neutrophils in systemic anaphylaxis in the rabbit
| dc.contributor.advisor | Halonen, Marilyn | en_US |
| dc.contributor.author | Dunn, Anita Marie, 1956- | |
| dc.creator | Dunn, Anita Marie, 1956- | en_US |
| dc.date.accessioned | 2013-03-28T10:23:43Z | en |
| dc.date.available | 2013-03-28T10:23:43Z | en |
| dc.date.issued | 1989 | en_US |
| dc.identifier.uri | http://hdl.handle.net/10150/276960 | en |
| dc.description.abstract | The objective of this study was to determine whether neutrophils play a significant role in anaphylaxis or in the response to the anaphylactic mediator platelet activating factor (PAF) in the rabbit. Vinblastine and anti-neutrophil antibodies were compared as neutrophil depleting agents, and 0.35 mg/kg vinblastine was selected as optimal for efficiency and specificity of depletion. Anaphylaxis was induced in sensitized rabbits by intravenous antigen challenge. Neutrophil depletion to 399 ± 101 cells/mm³ blood (14 ± 3%) did not significantly inhibit the physiologic and hematologic events associated with anaphylaxis except tachycardia. However, vinblastine pretreatment significantly reduced tachycardia and the right ventricular pressure increase and abolished the increase in pulmonary resistance caused by intravenous PAF. We conclude that although neutrophils do not play a significant role in IgE-anaphylaxis, they are important in the PAF-induced increases in right ventricular pressure and pulmonary resistance. PAF may not be a major mediator of these two physiologic alterations in IgE-anaphylaxis. | |
| dc.language.iso | en_US | en_US |
| dc.publisher | The University of Arizona. | en_US |
| dc.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. | en_US |
| dc.subject | Anaphylaxis. | en_US |
| dc.subject | Neutrophils. | en_US |
| dc.subject | Platelet activating factor. | en_US |
| dc.subject | Immunoglobulin E. | en_US |
| dc.title | The role of neutrophils in systemic anaphylaxis in the rabbit | en_US |
| dc.type | text | en_US |
| dc.type | Thesis-Reproduction (electronic) | en_US |
| dc.identifier.oclc | 22461871 | en_US |
| thesis.degree.grantor | University of Arizona | en_US |
| thesis.degree.level | masters | en_US |
| dc.identifier.proquest | 1336547 | en_US |
| thesis.degree.discipline | Graduate College | en_US |
| thesis.degree.discipline | Microbiology and Immunology | en_US |
| thesis.degree.name | M.S. | en_US |
| dc.identifier.bibrecord | .b17435729 | en_US |
| refterms.dateFOA | 2018-08-14T23:04:36Z | |
| html.description.abstract | The objective of this study was to determine whether neutrophils play a significant role in anaphylaxis or in the response to the anaphylactic mediator platelet activating factor (PAF) in the rabbit. Vinblastine and anti-neutrophil antibodies were compared as neutrophil depleting agents, and 0.35 mg/kg vinblastine was selected as optimal for efficiency and specificity of depletion. Anaphylaxis was induced in sensitized rabbits by intravenous antigen challenge. Neutrophil depletion to 399 ± 101 cells/mm³ blood (14 ± 3%) did not significantly inhibit the physiologic and hematologic events associated with anaphylaxis except tachycardia. However, vinblastine pretreatment significantly reduced tachycardia and the right ventricular pressure increase and abolished the increase in pulmonary resistance caused by intravenous PAF. We conclude that although neutrophils do not play a significant role in IgE-anaphylaxis, they are important in the PAF-induced increases in right ventricular pressure and pulmonary resistance. PAF may not be a major mediator of these two physiologic alterations in IgE-anaphylaxis. |
