UBC Theses and Dissertations
Investigating the transition from passive to active expiration in rodents Jenkin, Sarah Eleanor Maclay
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 expiratory phase duration (TE). This thesis highlights that AE is a flexible process, which can influence the breathing response in multiple ways (control of VT vs. control of TE). This suggests that the removal of the inhibitory inputs to the expiratory neural regions likely occurs through different mechanisms under different circumstances.
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