Investigating the transition from passive to active expiration in rodents
department or school: Science, Faculty of
data provider: DSpace
degree campus: UBCV
creator: Jenkin, Sarah Eleanor Maclay
issued: 2017-01-21T04:02:57
issued: 2016
related degree: Doctor of Philosophy - PhD
degree grantor: University of British Columbia
description: Under eupneic conditions, the breathing cycle is composed of three phases: inspiration (I), expiratory braking (E1) and a secondary expiratory phase (E2) during which there may be passive expiration and potentially an expiratory pause. Thus, inspiration is active and expiration is passive. With elevated respiratory drive, the abdominal muscles are recruited to exhale air forcefully from the lungs, producing active expiration (AE). Breathing is a highly integrated response, dependent on peripheral and central feedback. What is required to successfully transition from a passive to an active expiration is still unknown. The goal of this thesis was to determine what stimuli are required to recruit AE using a comparative approach. We determined which stimuli recruit AE, where within the breathing cycle AE occurs (early-expiration or late-expiration), and how the breathing cycle accommodates this new phase. Three different rat preparations (in vivo, in situ, and in vitro) were used to determine how anesthesia, afferent vagal feedback and peripheral and central chemoreceptors contribute to the production of AE. Hypoxia, anesthesia and afferent vagal feedback inhibited AE, while hypercapnia recruited AE. Central chemoreceptors were necessary to produce AE in vivo, but were insufficient to recruit AE in vitro. Within the pons, the Kölliker-Fuse actively inhibited the onset of AE activity, but did not directly initiate AE. Hypercapnia increased tidal volume (VT) and produced AE in all rodent species studied. However, there were differences in what CO₂ levels recruited AE, and where AE occurred within the breathing cycle. Most species recruited a late-expiratory AE, while agoutis, with elevated breathing frequencies and high dynamic compliance, recruited an early-expiratory AE. While AE can recruit the expiratory reserve volume to enhance VT in all species studied, the early-expiratory AE may enhance airflow to overcome an expiratory time constant that approaches the full expi…
aggregated CHO: https://circle.library.ubc.ca/rest/handle/2429/60154
note: INVESTIGATING THE TRANSITION FROM PASSIVE TO ACTIVE EXPIRATION IN RODENTS by Sarah Eleanor Maclay Jenkin B.Sc., The University of Guelph, 2009 M.Sc., The University of Toronto, 2011 A THESIS SUBMITTED IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF DOCTOR OF PHILOSOPHY in THE FACULTY OF GRADUATE AND POSTDOCTORAL STUDIES (Zoology) THE UNIVERSITY OF BRITISH COLUMBIA (Vancouver) December 2016 © Sarah Eleanor Maclay Jenkin, 2016 ii Abstract Under eupneic conditions, the breathing cycle is composed of three phases: inspiration (I), expiratory braking (E1) and a secondary expiratory phase (E2) during which there may be passive expiration and potentially an expiratory pause. Thus, inspiration is active and expiration is passive. With elevated respiratory drive, the abdominal muscles are recruited to exhale air forcefully from the lungs, producing active expiration (AE). Breathing is a highly integrated response, dependent on peripheral and central feedback. What is required to successfully transition from a passive to an active expiration is still unknown. The goal of this thesis was to determine what stimuli are required to recruit AE using a comparative approach. We determined which stimuli recruit AE, where within the breathing cycle AE occurs (early-expiration or late-expiration), and how the breathing cycle accommodates this new phase. Three different rat preparations (in vivo, in situ, and in vitro) were used to determine how anesthesia, afferent vagal feedback and peripheral and central chemoreceptors contribute to the production of AE. Hypoxia, anesthesia and afferent vagal feedback inhibited AE, while hypercapnia recruited AE. Central chemoreceptors were necessary to produce AE in vivo, but were insufficient to recruit AE in vitro. Within the pons, the Kölliker-Fuse actively inhibited the onset of AE activity, but did not directly initiate AE. Hypercapnia increased tidal volume (VT) and produced AE in all rodent species studied. However, there were di…
has type: Thesis/Dissertation
date issued: 2017-02
is shown at: 10.14288/1.0340510
language: eng
degree discipline: Zoology
provider: Vancouver : University of British Columbia Library
publisher: University of British Columbia
rights: Attribution-NonCommercial-NoDerivatives 4.0 International
rights URI: http://creativecommons.org/licenses/by-nc-nd/4.0/
scholar level: Graduate
type: Text
identifier URI: http://hdl.handle.net/2429/60154