Abstract
Sleep disordered breathing (SDB) is characterised by chronic intermittent asphyxia (CIA) due to repetitive apnoeas. We tested the hypothesis that CIA affects upper airway muscle activity and responses to acute hypoxia and asphyxia. Wistar rats were placed in restrainers with their heads in hoods ventilated with air (controls, n = 6) or an air/N2/CO2 mixture intermittently (treated group, n = 6) for 8 h per day, 5 days per week for 5 weeks using timed solenoid valves as previously described [1]. In were added to the the treated group, every 30 s, N2 and CO2 to a minimum of 6–8% and airflow for 15 s reducing hood O2 increasing CO2 to a maximum of 12–14% followed by removal of the N2 and CO2 and recovery to room air values. After 5 weeks, animals were anaesthetised (chloralose and urethane, 100 and 1000 mg/kg respectively IP). Sternohyoid (SH) electromyogram (EMG) activity was measured breathing air, 7.5% O2 in N2 (hypoxia) and 7.5% O2 and 3% CO2 (asphyxia). EMG data were expressed as % of peak activity breathing 9% CO2 (% of reference). Baseline SHEMG activity was significantly elevated in the treated group (28.4 ± 0.3% of reference in the controls vs. 48.5 ± 0.5% of reference in the treated group; means ± SEM, P < 0.05 ANOVA). CIA significantly reduced SHEMG responses to hypoxia and asphyxia. Thus, the increase in EMG activity from baseline values (ΔEMG) during the first minute of hypoxia was +46.2 ± 5.8% in control rats vs. +30.4 ± 6.1% in treated rats. Similarly, ΔEMG during the first minute of asphyxia was +66.3 ± 5.9% in control rats vs. +41.1 ± 11.1% in treated rats. We suggest that the elevated upper airway muscle activity associated with SDB is due to CIA. We propose that a reduction in the response of upper airway dilator muscles to acute asphyxia following upper airway obstruction is likely to cause further asphyxic insult leading to a vicious feed-forward cycle. We further propose that CIA contributes to the pathophysiology of SDB and other conditions of intermittent asphyxia.
Highlights
To be effective, inspiratory muscles on the left and right sides must contract together
We have found that a prominent gap in the column of ventral respiratory group (VRG) The nucleus tractus solitarii (NTS) relays information from primary related parvalbumin cells [2] likely corresponds to the pBc since visceral receptors to the central nervous system and is critically parvalbumin cells are rare in this zone and never co-localize with involved in the reflex control of autonomic functions
The specific protein(s) necessary for longterm facilitation (LTF) is unknown, we recently found that episodic hypoxia and LTF are associated with elevations in ventral spinal concentrations of brain derived neurotrophic factor (BDNF)
Summary
Inspiratory muscles on the left and right sides must contract together. The left and right halves of the diaphragm are synchronised because a bilateral population of medullary premotor neurones [1] simultaneously excites left and right phrenic motoneurones. Transection studies demonstrate that each side of the brainstem is capable of generating respiratory rhythm independently [2], so that left and right medullary inspiratory neurones must themselves be synchronised. The interconnections and common excitation that accomplish such synchronisation are unknown in rats. The respiratory rhythm of hypoglossal (XII) nerve discharge in transverse medullary slice preparations from neonatal rats is thought to originate in the region of the ventral respiratory group (VRG); generated there by a combination of “pacemaker” neurones [1] and their interactions with other respiratory neurones. Our goal was to discover interconnections between left and right VRG neurones as well as their connections to XII motoneurones
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