Smith, Julie Ann; (1993) The effects of mild hypoxia on hypoglossal motoneurones in neonates. Doctoral thesis (Ph.D), UCL (University College London).

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Abstract

The patency of the upper airway is dependent on the activity of the genioglossus muscle, the main protrusor muscle of the tongue. The force generated by this muscle opposes the negative intraluminal pressure produced by the contraction of the diaphragm during inspiration. Recent studies suggest that there is an immaturity in genioglossus muscle control in neonates and obstructive apnoea may occur when the activity of this muscle is reduced or absent without a corresponding decrease in the activity of the diaphragm. However, little is known of the processes mediating and influencing the activity of the hypoglossal nerve, the motor nerve of the genioglossus muscle, at this stage in development. In newborn babies, central apnoea (when there is no inspiratory effort) is usually followed by obstructive apnoea (when although there is inspiratory effort there is no inspiratory flow). It is therefore possible that hypoxia which develops during central apnoea, inhibits the activity of the genioglossus muscle and as a consequence the airway becomes obstructed. The aim of this study was therefore to determine whether hypoglossal motoneurones are inhibited during hypoxia in neonates. This study has investigated the effect of mild levels of hypoxaemia (PaO2 47.2 ± 3.8mmHg) on the activity of hypoglossal motoneurones in anaesthetized neonatal kittens (27 days old). The results showed that the majority of hypoglossal motoneurones increased in discharge frequency during hypoxia but for a substantial proportion the increase was only transient. Furthermore, some motoneurones showed a decrease in discharge frequency. Intracellular recordings showed that during similar levels of hypoxia, although a large proportion of the motoneurones were depolarized, at least some of these repolarized despite the continuing hypoxia. In addition, some hypoglossal motoneurones were hyperpolarized. This is the clearest evidence that inhibitory mechanisms, in addition to excitatory mechanisms, mediate the effects of hypoxia on hypoglossal output in neonates. Furthermore, the results suggest that hypoxia has an effect on the hypoglossal motoneurones independently of, or in addition to, its effect through respiratory rhythm. In some preliminary studies, the transmembrane input resistance increased during the hyperpolarization in response to hypoxia. One possibility is that the inhibition is mediated by the removal of an excitatory input. If the inhibition found in this study occurs in human babies it may be a compounding factor in apnoeas of the newborn.

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