Abstract
1. Following d-tuhocurarine, physostigmine restored both the phrenic nerve diaphragm and sciatic nerve-gastrocnemius twitches, recovery of the two preparations usually occurring simultaneously. The same restoration of neuromuscular transmission was seen upon injecting No. 49-204 during the myoneural blockade by decamethonium.
2. After high dosage with either of the three blocking agents which were studied, the return of the diaphragmatic twitch on stimulation of the phrenic nerve occurred appreciably before resumption of spontaneous respiration, whether this return of myoneural transmission took place with or without use of such antagonists as physostigmine for d-tubocurarine or No. 49-204 for decamethonium.
3. During the period between return of the phrenic nerve-diaphragm twitch and the return of spontaneous respiration, lobeline or TRC-209 caused an instantaneous resumption of respiratory movements.
4. During the period between return of the phrenic nerve-diaphragm twitch and the return of spontaneous respiration, phrenic nerve action potentials were shown to be absent, their return coinciding with the reappearance of spontaneous respiratory movements.
5. The conclusion is drawn that the protracted respiratory arrest which persists well after restoration of functional neuromuscular transmission must be due to a depressant action of these agents on either the respiratory center or on other nervous elements central to the phrenic nerve. Whether this is a direct action of the drugs or an indirect action resulting from anoxia or some other related phenomenon is not established.
Footnotes
- Received August 1, 1952.
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