Document Detail


Phasic respiratory modulation of pharyngeal collapsibility via neuromuscular mechanisms in rats.
MedLine Citation:
PMID:  22052868     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Obstructive sleep apnea patients experience recurrent upper airway (UA) collapse due to decreases in the UA dilator muscle activity during sleep. In contrast, activation of UA dilators reduces pharyngeal critical pressure (Pcrit, an index of pharyngeal collapsibility), suggesting an inverse relationship between pharyngeal collapsibility and dilator activity. Since most UA muscles display phasic respiratory activity, we hypothesized that pharyngeal collapsibility is modulated by respiratory drive via neuromuscular mechanisms. Adult male Sprague-Dawley rats were anesthetized, vagotomized, and ventilated (normocapnia). In one group, integrated genioglossal activity, Pcrit, and maximal airflow (V(max)) were measured at three expiration and five inspiration time points within the breathing cycle. Pcrit was closely and inversely related to phasic genioglossal activity, with the value measured at peak inspiration being the lowest. In other groups, the variables were measured during expiration and peak inspiration, before and after each of five manipulations. Pcrit was 26% more negative (-15.0 ± 1.0 cmH(2)O, -18.9 ± 1.2 cmH(2)O; n = 23), V(max) was 7% larger (31.0 ± 1.0 ml/s, 33.2 ± 1.1 ml/s), nasal resistance was 12% bigger [0.49 ± 0.05 cmH(2)O/(ml/s), 0.59 ± 0.05 cmH(2)O/(ml/s)], and latency to induced UA closure was 14% longer (55 ± 4 ms, 63 ± 5 ms) during peak inspiration vs. expiration (all P < 0.005). The expiration-inspiration difference in Pcrit was abolished with neuromuscular blockade, hypocapnic apnea, or death but was not reduced by the superior laryngeal nerve transection or altered by tracheal displacement. Collectively, these results suggest that pharyngeal collapsibility is moment-by-moment modulated by respiratory drive and this phasic modulation requires neuromuscular mechanisms, but not the UA negative pressure reflex or tracheal displacement by phasic lung inflation.
Authors:
Ying Cao; Michelle McGuire; Chun Liu; Atul Malhotra; Liming Ling
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-11-03
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  112     ISSN:  1522-1601     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2012 Mar 
Date Detail:
Created Date:  2012-03-02     Completed Date:  2012-09-11     Revised Date:  2013-11-11    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  695-703     Citation Subset:  IM    
Affiliation:
Division of Sleep Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apnea / physiopathology
Electromyography / methods
Laryngeal Nerve Injuries / physiopathology*
Lung / drug effects,  physiopathology*
Male
Neuromuscular Blockade
Neuromuscular Junction / drug effects,  physiopathology*
Pharynx / drug effects,  innervation*,  physiopathology*
Rats
Rats, Sprague-Dawley
Respiration / drug effects
Respiratory Mechanics / physiology*
Sleep Apnea, Obstructive / physiopathology
Trachea / drug effects,  physiopathology*
Ventilators, Negative-Pressure
Grant Support
ID/Acronym/Agency:
HL-64912/HL/NHLBI NIH HHS; K24 HL093218/HL/NHLBI NIH HHS; K24-HL-093218/HL/NHLBI NIH HHS; P01 HL095491/HL/NHLBI NIH HHS; P01-HL-095491/HL/NHLBI NIH HHS; R01 HL085188/HL/NHLBI NIH HHS; R01 HL090897/HL/NHLBI NIH HHS; R01-HL-085188/HL/NHLBI NIH HHS; R01-HL090897/HL/NHLBI NIH HHS
Comments/Corrections

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