AI Article Synopsis
- The study examined how ketamine affects the mylohyoid nerve and phrenic nerves in rabbits that were anesthetized and artificially ventilated.
- Ketamine prolonged the phrenic nerve's inspiratory activity but reduced the mylohyoid nerve's expiratory activity, demonstrating its influence on respiratory patterns.
- The results suggest that ketamine inhibits a key motor nucleus in the Vth nerve, impacting both inspiratory and expiratory respiratory control mechanisms.
Article Abstract
The effects of ketamine on the activities of the mylohyoid nerve (a branch of the Vth nerve) and of both phrenic nerves were investigated in rabbits anaesthetized with halothane, paralyzed and artificially ventilated. Intravenous administration of ketamine elicited a marked prolongation of the phrenic inspiratory discharge (without significantly affecting its amplitude) and a depression of the mylohyoid expiratory activity. An elimination of the volume-related input from the lungs ("no-inflation manoeuvre") or deflation elicited under these conditions typical apneustic pattern of breathing. The response to tracheal occlusion at peak-inspiration was "classical". We conclude that ketamine inhibits the Vth nerve motor nucleus which is not only an important component of the central inspiratory-inhibitory neurones but also a "relay station" between the vagal and the central inspiratory "off-switch" mechanisms.
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