Abstract
1. Electroneurographical (ENG) activities of a phrenic nerve, a thyroarytenoid (TA) branch of a recurrent laryngeal nerve, and a triangularis sterni (TS) branch of an internal intercostal nerve were recorded in decerebrate, vagotomized and paralysed cats. A superior laryngeal nerve (SLN) was stimulated electrically. Our objective was to evaluate transient changes in motor activity following a brief perturbation of the respiratory cycle by SLN stimulation. 2. Each motor nerve recorded represents a separate phase of the respiratory cycle. We measured the duration of phrenic ENG activity for inspiratory phase duration (TI) and similarly the duration of TA and TS ENG activity for the duration of stages I and II of expiration, respectively. Changes in the duration of the total respiratory cycle (TTOT) were also measured. Therefore, the changes in TTOT were accounted for directly by changes in each phase of the respiratory cycle. 3. Perturbation during the inspiratory phase inhibited phrenic activity either reversibly or irreversibly (premature termination of inspiration) depending on the strength and timing of the stimulus. Reversible inhibition of inspiration was associated with a transient activation (< 100 ms) of the TA nerve followed by a reactivation of the phrenic nerve, but the duration of the subsequent stages I and II of expiration remained the same. Thus, the prolongation of TTOT was completely accounted for by the lengthening of TI. 4. Premature termination of inspiration was followed by either a shortening (the first half of inspiration) or a lengthening (the second half of inspiration) of the duration of stage I expiration and consistently by a shortening of the duration of stage II expiration. The magnitude of these changes in the durations of stages I and II of expiration was phase dependent. Changes in the duration of all three phases of motor activity contributed to the changes in TTOT. 5. Perturbation during stage I expiration prolonged this stage but did not affect the duration of the succeeding stage (stage II expiration). The increase in the duration of stage I expiration appeared constant and not dependent on the time when the perturbation was delivered in stage I expiration. Thus, the change in TTOT was less phase dependent during stage I expiration than during inspiration and stage II expiration and was accounted for by changes in the duration of TA activity alone. 6. Perturbation during stage II expiration inhibited TS activity and evoked TA activity transiently.(ABSTRACT TRUNCATED AT 400 WORDS)
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