Recovery from central apnea: Effect of stimulus duration and end-tidal CO2 partial pressure

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Abstract

The present study was designed to investigate the effect of stimulus duration and chemosensory input on the recovery of central respiratory activity from apnea induced by superior laryngeal nerve (SLN) electrical stimulation. Newborn piglets less than 8 days of age were anesthetized, paralyzed, and mechanically ventilated at differing levels of end-tidal CO2 partial pressure (P(CO2)). The vagi were cut bilaterally in the neck. Integrated phrenic nerve activity was used as the index of respiratory activity. SLN stimulation caused apnea that persisted after stimulus cessation. The length of apnea following stimulus cessation was directly related to stimulus duration and inversely related to end-tidal P(CO2). After apnea, respiratory activity returned gradually to the initial control level. The recovery pattern was well described by a linear regression function using the natural logarithm of time as the independent variable. Prolonging stimulus duration progressively inhibited the amount of initial respiratory activity following apnea. On the other hand, the rate of respiratory recovery was independent of stimulus duration and, except at low end-tidal P(CO2) following long (30 s) stimuli, was independent of the end-tidal P(CO2) level. These results demonstrate that a long-acting central mechanism regulates recovery from apnea induced by SLN stimulation.

Original languageEnglish (US)
Pages (from-to)105-109
Number of pages5
JournalJournal of Applied Physiology Respiratory Environmental and Exercise Physiology
Volume53
Issue number1
StatePublished - 1982
Externally publishedYes

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Central Sleep Apnea
Partial Pressure
Apnea
Laryngeal Nerves
Phrenic Nerve
Respiratory Rate
Electric Stimulation
Linear Models
Neck

ASJC Scopus subject areas

  • Endocrinology
  • Physiology

Cite this

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title = "Recovery from central apnea: Effect of stimulus duration and end-tidal CO2 partial pressure",
abstract = "The present study was designed to investigate the effect of stimulus duration and chemosensory input on the recovery of central respiratory activity from apnea induced by superior laryngeal nerve (SLN) electrical stimulation. Newborn piglets less than 8 days of age were anesthetized, paralyzed, and mechanically ventilated at differing levels of end-tidal CO2 partial pressure (P(CO2)). The vagi were cut bilaterally in the neck. Integrated phrenic nerve activity was used as the index of respiratory activity. SLN stimulation caused apnea that persisted after stimulus cessation. The length of apnea following stimulus cessation was directly related to stimulus duration and inversely related to end-tidal P(CO2). After apnea, respiratory activity returned gradually to the initial control level. The recovery pattern was well described by a linear regression function using the natural logarithm of time as the independent variable. Prolonging stimulus duration progressively inhibited the amount of initial respiratory activity following apnea. On the other hand, the rate of respiratory recovery was independent of stimulus duration and, except at low end-tidal P(CO2) following long (30 s) stimuli, was independent of the end-tidal P(CO2) level. These results demonstrate that a long-acting central mechanism regulates recovery from apnea induced by SLN stimulation.",
author = "Edward Lawson",
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journal = "Journal of Applied Physiology",
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TY - JOUR

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T2 - Effect of stimulus duration and end-tidal CO2 partial pressure

AU - Lawson, Edward

PY - 1982

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N2 - The present study was designed to investigate the effect of stimulus duration and chemosensory input on the recovery of central respiratory activity from apnea induced by superior laryngeal nerve (SLN) electrical stimulation. Newborn piglets less than 8 days of age were anesthetized, paralyzed, and mechanically ventilated at differing levels of end-tidal CO2 partial pressure (P(CO2)). The vagi were cut bilaterally in the neck. Integrated phrenic nerve activity was used as the index of respiratory activity. SLN stimulation caused apnea that persisted after stimulus cessation. The length of apnea following stimulus cessation was directly related to stimulus duration and inversely related to end-tidal P(CO2). After apnea, respiratory activity returned gradually to the initial control level. The recovery pattern was well described by a linear regression function using the natural logarithm of time as the independent variable. Prolonging stimulus duration progressively inhibited the amount of initial respiratory activity following apnea. On the other hand, the rate of respiratory recovery was independent of stimulus duration and, except at low end-tidal P(CO2) following long (30 s) stimuli, was independent of the end-tidal P(CO2) level. These results demonstrate that a long-acting central mechanism regulates recovery from apnea induced by SLN stimulation.

AB - The present study was designed to investigate the effect of stimulus duration and chemosensory input on the recovery of central respiratory activity from apnea induced by superior laryngeal nerve (SLN) electrical stimulation. Newborn piglets less than 8 days of age were anesthetized, paralyzed, and mechanically ventilated at differing levels of end-tidal CO2 partial pressure (P(CO2)). The vagi were cut bilaterally in the neck. Integrated phrenic nerve activity was used as the index of respiratory activity. SLN stimulation caused apnea that persisted after stimulus cessation. The length of apnea following stimulus cessation was directly related to stimulus duration and inversely related to end-tidal P(CO2). After apnea, respiratory activity returned gradually to the initial control level. The recovery pattern was well described by a linear regression function using the natural logarithm of time as the independent variable. Prolonging stimulus duration progressively inhibited the amount of initial respiratory activity following apnea. On the other hand, the rate of respiratory recovery was independent of stimulus duration and, except at low end-tidal P(CO2) following long (30 s) stimuli, was independent of the end-tidal P(CO2) level. These results demonstrate that a long-acting central mechanism regulates recovery from apnea induced by SLN stimulation.

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