Regulation of microvascular permeability during histamine stimulation in rat mesentery.

Persistent Link:
http://hdl.handle.net/10150/185367
Title:
Regulation of microvascular permeability during histamine stimulation in rat mesentery.
Author:
Wu, Ning Zhong.
Issue Date:
1991
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:
Histamine is known to cause a substantial increase in the permeability of venules to both water and proteins. However, this increase is transient, i.e. the initially elevated permeability escapes even during continuous histamine stimulation. This project was designed to identify the mechanisms underlying this permeability-escape phenomenon. The project was conducted in two stages. In the first stage, three series of experiments were performed to test the hypothesis that the permeability-escape phenomenon is due to the reclosure of endothelial gaps. Firstly, the time course of permeability changes to a-lactalbumin during continuous histamine stimulation was obtained from single venules of rat mesentery. It was found that, after the start of histamine treatment, permeability initially increased, peaked around the third minute and then declined towards its control level. Secondly, the temporal development of endothelial gaps during histamine treatment was studied with electron microscopy. The number of gaps underwent a similar development, i.e. an initial increase, peaking at 3 minutes, and a subsequent decrease toward control. Lastly, both permeability and gap morphology were obtained from the same individual venules subjected to different periods of histamine treatment. It was found that the temporal development of the gaps was mirrored by that of permeability. Since both permeability and endothelial gaps followed similar developmental patterns during histamine treatment, the result supports the hypothesis that the permeability-escape phenomenon is due to the reclosure of endothelial gaps. In the second stage, the chemical signal initiating the permeability escape was identified. Specifically, we tested whether histamine's binding to H2 receptors and/or the production of prostacyclin by endothelial cells were involved. The time course of venular permeability changes during histamine stimulation was measured in the presence of H2 receptor antagonist and of prostacyclin synthetase inhibitor, respectively. It was found that, while blocking H2 receptors did not have any effect on the escape of permeability, inhibiting prostacyclin synthesis suppressed or even abolished the permeability-escape phenomenon. Therefore, we concluded that the production of prostacyclin by endothelial cells may serve as one chemical signal to initiate the escape of permeability.
Type:
text; Dissertation-Reproduction (electronic)
Keywords:
Dissertations, Academic; Cells -- Permeability.
Degree Name:
Ph.D.
Degree Level:
doctoral
Degree Program:
Physiological Sciences; Graduate College
Degree Grantor:
University of Arizona
Advisor:
Baldwin, Ann

Full metadata record

DC FieldValue Language
dc.language.isoenen_US
dc.titleRegulation of microvascular permeability during histamine stimulation in rat mesentery.en_US
dc.creatorWu, Ning Zhong.en_US
dc.contributor.authorWu, Ning Zhong.en_US
dc.date.issued1991en_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.abstractHistamine is known to cause a substantial increase in the permeability of venules to both water and proteins. However, this increase is transient, i.e. the initially elevated permeability escapes even during continuous histamine stimulation. This project was designed to identify the mechanisms underlying this permeability-escape phenomenon. The project was conducted in two stages. In the first stage, three series of experiments were performed to test the hypothesis that the permeability-escape phenomenon is due to the reclosure of endothelial gaps. Firstly, the time course of permeability changes to a-lactalbumin during continuous histamine stimulation was obtained from single venules of rat mesentery. It was found that, after the start of histamine treatment, permeability initially increased, peaked around the third minute and then declined towards its control level. Secondly, the temporal development of endothelial gaps during histamine treatment was studied with electron microscopy. The number of gaps underwent a similar development, i.e. an initial increase, peaking at 3 minutes, and a subsequent decrease toward control. Lastly, both permeability and gap morphology were obtained from the same individual venules subjected to different periods of histamine treatment. It was found that the temporal development of the gaps was mirrored by that of permeability. Since both permeability and endothelial gaps followed similar developmental patterns during histamine treatment, the result supports the hypothesis that the permeability-escape phenomenon is due to the reclosure of endothelial gaps. In the second stage, the chemical signal initiating the permeability escape was identified. Specifically, we tested whether histamine's binding to H2 receptors and/or the production of prostacyclin by endothelial cells were involved. The time course of venular permeability changes during histamine stimulation was measured in the presence of H2 receptor antagonist and of prostacyclin synthetase inhibitor, respectively. It was found that, while blocking H2 receptors did not have any effect on the escape of permeability, inhibiting prostacyclin synthesis suppressed or even abolished the permeability-escape phenomenon. Therefore, we concluded that the production of prostacyclin by endothelial cells may serve as one chemical signal to initiate the escape of permeability.en_US
dc.typetexten_US
dc.typeDissertation-Reproduction (electronic)en_US
dc.subjectDissertations, Academicen_US
dc.subjectCells -- Permeability.en_US
thesis.degree.namePh.D.en_US
thesis.degree.leveldoctoralen_US
thesis.degree.disciplinePhysiological Sciencesen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.grantorUniversity of Arizonaen_US
dc.contributor.advisorBaldwin, Annen_US
dc.contributor.committeememberBurt, Janisen_US
dc.contributor.committeememberKatz, Murrayen_US
dc.contributor.committeememberMcCuskey, Roberten_US
dc.contributor.committeememberSchaeffer, Richarden_US
dc.identifier.proquest9121554en_US
dc.identifier.oclc709606324en_US
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