Neurocirculatory consequences of negative intrathoracic pressure vs. asphyxia during voluntary apnea. J Appl Physiol (1985) 1993 Jun;74(6):2969-75
Date
06/01/1993Pubmed ID
8365996DOI
10.1152/jappl.1993.74.6.2969Scopus ID
2-s2.0-0027246421 (requires institutional sign-in at Scopus site) 172 CitationsAbstract
To investigate the mechanisms responsible for fluctuations in arterial pressure and sympathetic nerve activity that occur during obstructive sleep apnea, we studied neurocirculatory responses to Mueller maneuvers and breath holds in conscious humans. During 20-s Mueller maneuvers at -40 mmHg, mean arterial pressure fell initially (-11 +/- 3 mmHg) and then rose above baseline (+8 +/- 3 mmHg) on release of the inspiratory strain. Sympathetic outflow to skeletal muscle was almost completely suppressed during the initial moments of the maneuver and rose to more than three times the baseline level at the termination of the maneuver. Simple 20-s breath holds were accompanied by time-dependent increases in both arterial pressure (+11 +/- 3 mmHg) and sympathetic nerve activity (> 3 times baseline). The administration of supplemental O2 greatly attenuated the increases in arterial pressure and sympathetic nerve activity during Mueller maneuvers and breath holds. We conclude that carotid chemoreflex stimulation is the primary mechanism responsible for apnea-induced sympathetic activation during wakefulness and that it may contribute importantly to the sympathetic activation that accompanies sleep-disordered breathing.
Author List
Morgan BJ, Denahan T, Ebert TJAuthor
Thomas J. Ebert MD, PhD Adjunct Professor in the Anesthesiology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AdultAirway Resistance
Apnea
Asphyxia
Blood Pressure
Chemoreceptor Cells
Electrophysiology
Humans
Male
Middle Aged
Oxygen
Pressoreceptors
Pressure
Reflex
Sympathetic Nervous System
