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Cervical sympathetic and phrenic nerve responses to progressive brain hypoxia

  • M. J. Wasicko
  • , J. E. Melton
  • , J. A. Neubauer
  • , N. Krawciw
  • , N. H. Edelman
  • Rutgers - The State University of New Jersey, New Brunswick

Research output: Contribution to journalArticlepeer-review

24 Scopus citations

Abstract

To determine if depression of central respiratory output during progressive brain hypoxia (PBH) can be generalized to other brain stem outputs, we examined the effect of PBH on the tonic (tSCS) and inspiratory-synchronous (iSCS) components of preganglionic superior cervical sympathetic (SCS) nerve activity. Peak phrenic and SCS activity were measured in nine anesthetized, paralyzed, peripherally chemodenervated, vagotomized cats. PBH was produced by inhalation of 0.5% CO in 40% O2 while blood pressure and end-tidal CO2 were maintained constant. A progressive reduction in arterial O2 content from 14.3 ± 0.6 to 4.5 ± 0.3 vol% caused a 79 ± 7% depression of peak phrenic activity and an 84 ± 10% reduction of iSCS activity, but tSCS activity increased 42 ± 21%. During CO2 rebreathing, iSCS activity increased in parallel with peak phrenic activity while tSCS activity was unchanged. The slopes of the CO2 responses of both phrenic (6.3 ± 1.2% max/mmHg) and iSCS (4.6 ± 0.8% max/mmHg) activity were unaffected by PBH. In four of nine hypocapnic and three of nine hypoxic studies, inspiratory activity in the SCS nerve was observed event after completely silencing the phrenic neurogram. We conclude that 1) the increase in tSCS activity seen during PBH in this model suggests that in the range studied hypoxia may not be a general depressant of brain stem output, 2) the observation that changes in the magnitude of iSCS activity parallel changes in phrenic amplitude suggests that common circuits generate phrenic and iSCS activity (however, the presence of iSCS activity during hypocapnic or hypoxic phrenic apnea suggests that phrenic and SCS outputs may be differentially gated with regard to a common neural oscillator), and 3) because, as previously shown for phrenic activity, PBH does not depress the CO2 response of the iSCS activity, we conclude that hypoxia does not functionally impair the neurons involved in generating inspiratory-synchronous sympathetic activity.

Original languageEnglish
Pages (from-to)53-58
Number of pages6
JournalJournal of Applied Physiology
Volume68
Issue number1
DOIs
StatePublished - 1990

Keywords

  • carboxyhemoglobinemia
  • cat
  • hypoxic respiratory depression
  • respiratory-sympathetic interaction

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