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  • 1
    Online Resource
    Online Resource
    American Physiological Society ; 2013
    In:  Journal of Applied Physiology Vol. 115, No. 3 ( 2013-08-01), p. 337-345
    In: Journal of Applied Physiology, American Physiological Society, Vol. 115, No. 3 ( 2013-08-01), p. 337-345
    Abstract: Increasing lung volume increases upper airway patency and decreases airway resistance and collapsibility. The role of diaphragm contraction in producing these changes remains unclear. This study was undertaken to determine the effect of selective diaphragm contraction, induced by phrenic nerve stimulation, on upper airway collapsibility and the extent to which any observed change was attributable to lung volume-related changes in pressure gradients or to diaphragm descent-related mediastinal traction. Continuous bilateral transcutaneous cervical phrenic nerve stimulation (30 Hz) was applied to nine supine, anesthetized human subjects during transient decreases in airway pressure to levels sufficient to produce flow limitation when unstimulated. Stimulation was applied at two intensities (low and high) and its effects on lung volume and airflow quantified relative to unstimulated conditions. Lung volume increased by 386 ± 269 ml (means ± SD) and 761 ± 556 ml during low and high stimulation, respectively ( P 〈 0.05 for the difference between these values), which was associated with peak inspiratory flow increases of 69 ± 57 and 137 ± 108 ml/s, respectively ( P 〈 0.05 for the difference). Stimulation-induced change in lung volume correlated with change in peak flow ( r = 0.65, P 〈 0.01). Diaphragm descent-related outward displacement of the abdominal wall produced no change in airflow unless accompanied by lung volume change. We conclude that phrenic nerve stimulation-induced diaphragm contraction increases lung volume and reduces airway collapsibility in a dose-dependent manner. The effect appears primarily mediated by changes in lung volume rather than mediastinal traction from diaphragm descent. The study provides a rationale for use of continuous phrenic stimulation to treat obstructive sleep apnea.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2013
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 2
    Online Resource
    Online Resource
    American Physiological Society ; 2003
    In:  Journal of Applied Physiology Vol. 95, No. 1 ( 2003-07), p. 357-363
    In: Journal of Applied Physiology, American Physiological Society, Vol. 95, No. 1 ( 2003-07), p. 357-363
    Abstract: Upper airway (UA) patency may be influenced by surface tension (γ) operating within the (UAL). We examined the role of γ of UAL in the maintenance of UA patency in eight isoflurane-anesthetized supine human subjects breathing via a nasal mask connected to a pneumotachograph attached to a pressure delivery system. We evaluated 1) mask pressure at which the UA closed (Pcrit), 2) UA resistance upstream from the site of UA collapse (RUS), and 3) mask pressure at which the UA reopened (Po). A multiple pressure-transducer catheter was used to identify the site of airway closure (velopharyngeal in all subjects). UAL samples (0.2 μl) were collected, and the γ of UAL was determined by using the “pull-off force” technique. Studies were performed before and after the intrapharyngeal instillation of 5 ml of exogenous surfactant (Exosurf, Glaxo Smith Kline). The γ of UAL decreased from 61.9 ± 4.1 (control) to 50.3 ± 5.0 mN/m (surfactant; P 〈 0.02). Changes in Po, RUS, and Po - Pcrit (change = control - surfactant) were positively correlated with changes in γ ( r 2 〉 0.6; P 〈 0.02) but not with changes in Pcrit ( r 2 = 0.4; P 〉 0.9). In addition, mean peak inspiratory airflow (no flow limitation) significantly increased ( P 〈 0.04) from 0.31 ± 0.06 (control) to 0.36 ± 0.06 l/s (surfactant). These findings suggest that γ of UAL exerts a force on the UA wall that hinders airway opening. Instillation of exogenous surfactant into the UA lowers the γ of UAL, thus increasing UA patency and augmenting reopening of the collapsed airway.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2003
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 3
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2002
    In:  Anesthesiology Vol. 97, No. 4 ( 2002-10-01), p. 786-793
    In: Anesthesiology, Ovid Technologies (Wolters Kluwer Health), Vol. 97, No. 4 ( 2002-10-01), p. 786-793
    Abstract: The unprotected upper airway tends to obstruct during general anesthesia, yet its mechanical properties have not been studied in detail during this condition. Methods To study its collapsibility, pressure-flow relationships of the upper airway were obtained at three levels of anesthesia (end-tidal isoflurane = 1.2%, 0.8%, and 0.4%) in 16 subjects while supine and spontaneously breathing on nasal continuous positive airway pressure. At each level of anesthesia, mask pressure was transiently reduced from a pressure sufficient to abolish inspiratory flow limitation (11.8 +/- 2.7 cm H(2)O) to pressures resulting in variable degrees of flow limitation. The relation between mask pressure and maximal inspiratory flow was determined, and the critical pressure at which the airway occluded was recorded. The site of collapse was determined from simultaneous measurements of nasopharyngeal, oropharyngeal, and hypopharyngeal and esophageal pressures. Results The airway remained hypotonic (minimal or absent intramuscular genioglossus electromyogram activity) throughout each study. During flow-limited breaths, inspiratory flow decreased linearly with decreasing mask pressure (r(2) = 0.86 +/- 0.17), consistent with Starling resistor behavior. At end-tidal isoflurane of 1.2%, critical pressure was 1.1 +/- 3.5 cm H O; at 0.4% it decreased to -0.2 +/- 3.6 cm H(2)O ( & lt; 0.05), indicating decreased airway collapsibility. This decrease was associated with a decrease in end-expiratory esophageal pressure of 0.6 +/- 0.9 cm H(2)O ( & lt; 0.05), suggesting an increased lung volume. Collapse occurred in the retropalatal region in 14 subjects and in the retrolingual region in 2 subjects, and did not change with anesthetic depth. Conclusions Isoflurane anesthesia is associated with decreased muscle activity and increased collapsibility of the upper airway. In this state it adopts the behavior of a Starling resistor. The decreased collapsibility observed with decreasing anesthetic depth was not a consequence of neuromuscular activity, which was unchanged. Rather, it may be related to increased lung volume and its effect on airway wall longitudinal tension. The predominant site of collapse is the soft palate.
    Type of Medium: Online Resource
    ISSN: 0003-3022
    RVK:
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2002
    detail.hit.zdb_id: 2016092-6
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  • 4
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2010
    In:  Anesthesiology Vol. 112, No. 2 ( 2010-02-01), p. 497-497
    In: Anesthesiology, Ovid Technologies (Wolters Kluwer Health), Vol. 112, No. 2 ( 2010-02-01), p. 497-497
    Type of Medium: Online Resource
    ISSN: 0003-3022
    RVK:
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2010
    detail.hit.zdb_id: 2016092-6
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  • 5
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2005
    In:  Anesthesiology Vol. 103, No. 3 ( 2005-09-01), p. 470-477
    In: Anesthesiology, Ovid Technologies (Wolters Kluwer Health), Vol. 103, No. 3 ( 2005-09-01), p. 470-477
    Abstract: This study investigated the effect of varying concentrations of propofol on upper airway collapsibility and the mechanisms responsible for it. Methods Upper airway collapsibility was determined from pressure-flow relations at three concentrations of propofol anesthesia (effect site concentration = 2.5, 4.0, and 6.0 mug/ml) in 12 subjects spontaneously breathing on continuous positive airway pressure. At each level of anesthesia, mask pressure was transiently reduced from a pressure sufficient to abolish inspiratory flow limitation (maintenance pressure = 12 +/- 1 cm H2O) to pressures resulting in variable degrees of flow limitation. The relation between mask pressure and maximal inspiratory flow was determined, and the critical pressure at which the airway occluded was recorded. Electromyographic activity of the genioglossus muscle (EMGgg) was obtained via intramuscular electrodes in 8 subjects. Results With increasing depth of anesthesia, (1) critical closing pressure progressively increased (-0.3 +/- 3.5, 0.5 +/- 3.7, and 1.4 +/- 3.5 cm H2O at propofol concentrations of 2.5, 4.0, and 6.0 microg/ml respectively; P & lt; 0.05 between each level), indicating a more collapsible upper airway; (2) inspiratory flow at the maintenance pressure significantly decreased; and (3) respiration-related phasic changes in EMGgg at the maintenance pressure decreased from 7.3 +/- 9.9% of maximum at 2.5 microg/ml to 0.8 +/- 0.5% of maximum at 6.0 microg/ml, whereas tonic EMGgg was unchanged. Relative to the levels of phasic and tonic EMGgg at the maintenance pressure immediately before a decrease in mask pressure, tonic activity tended to increase over the course of five flow-limited breaths at a propofol concentration of 2.5 microg/ml but not at propofol concentrations of 4.0 and 6.0 microg/ml, whereas phasic EMGgg was unchanged. Conclusions Increasing depth of propofol anesthesia is associated with increased collapsibility of the upper airway. This was associated with profound inhibition of genioglossus muscle activity. This dose-related inhibition seems to be the combined result of depression of central respiratory output to upper airway dilator muscles and of upper airway reflexes.
    Type of Medium: Online Resource
    ISSN: 0003-3022
    RVK:
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2005
    detail.hit.zdb_id: 2016092-6
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  • 6
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2020
    In:  Anesthesia & Analgesia Vol. 130, No. 4 ( 2020-04), p. 1008-1017
    In: Anesthesia & Analgesia, Ovid Technologies (Wolters Kluwer Health), Vol. 130, No. 4 ( 2020-04), p. 1008-1017
    Abstract: The propensities for the upper airway to collapse during anesthesia and sleep are related, although much of our understanding of this relationship has been inferred from clinical observation and indirect measures such as the apnea–hypopnea index. The aim of this study was to use an identical, rigorous, direct measure of upper airway collapsibility (critical closing pressure of the upper airway) under both conditions to allow the magnitude of upper airway collapsibility in each state to be precisely compared. METHODS: Ten subjects (8 men and 2 women; mean ± SD: age, 40.4 ± 12.1 years; body mass index, 28.5 ± 4.0 kg/m 2 ) were studied. Critical closing pressure of the upper airway was measured in each subject on separate days during (1) propofol anesthesia and (2) sleep. RESULTS: Critical closing pressure of the upper airway measurements were obtained in all 10 subjects during nonrapid eye movement sleep and, in 4 of these 10 subjects, also during rapid eye movement sleep. Critical closing pressure of the upper airway during anesthesia was linearly related to critical closing pressure of the upper airway during nonrapid eye movement sleep ( r = 0.64 [95% CI, 0.02–0.91]; n = 10; P = .046) with a similar tendency in rapid eye movement sleep ( r = 0.80 [95% CI, −0.70 to 0.99]; n = 4; P = .200). However, critical closing pressure of the upper airway during anesthesia was systematically greater (indicating increased collapsibility) than during nonrapid eye movement sleep (2.1 ± 2.2 vs −2.0 ± 3.2 cm H 2 O, respectively, n = 10; within-subject mean difference, 4.1 cm H 2 O [95% CI, 2.32–5.87]; P 〈 .001) with a similar tendency during rapid eye movement sleep (1.6 ± 2.4 vs −1.9 ± 4.3 cm H 2 O, respectively, n = 4; unadjusted difference, 3.5 cm H 2 O [95% CI, −0.95 to 7.96]; P = .087). CONCLUSIONS: These results demonstrate that the magnitude of upper airway collapsibility during anesthesia and sleep is directly related. However, the upper airway is systematically more collapsible during anesthesia than sleep, suggesting greater vulnerability to upper airway obstruction in the anesthetized state.
    Type of Medium: Online Resource
    ISSN: 0003-2999
    RVK:
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
    detail.hit.zdb_id: 2018275-2
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  • 7
    Online Resource
    Online Resource
    Elsevier BV ; 2004
    In:  Sleep Medicine Reviews Vol. 8, No. 6 ( 2004-12), p. 459-471
    In: Sleep Medicine Reviews, Elsevier BV, Vol. 8, No. 6 ( 2004-12), p. 459-471
    Type of Medium: Online Resource
    ISSN: 1087-0792
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2004
    detail.hit.zdb_id: 2010032-2
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  • 8
    Online Resource
    Online Resource
    Elsevier BV ; 2010
    In:  Anesthesiology Clinics Vol. 28, No. 3 ( 2010-09), p. 443-455
    In: Anesthesiology Clinics, Elsevier BV, Vol. 28, No. 3 ( 2010-09), p. 443-455
    Type of Medium: Online Resource
    ISSN: 1932-2275
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2010
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  • 9
    Online Resource
    Online Resource
    Elsevier BV ; 2007
    In:  Seminars in Anesthesia, Perioperative Medicine and Pain Vol. 26, No. 2 ( 2007-6), p. 65-72
    In: Seminars in Anesthesia, Perioperative Medicine and Pain, Elsevier BV, Vol. 26, No. 2 ( 2007-6), p. 65-72
    Type of Medium: Online Resource
    ISSN: 0277-0326
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2007
    detail.hit.zdb_id: 2145877-7
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  • 10
    Online Resource
    Online Resource
    Elsevier BV ; 2002
    In:  The Lancet Vol. 359, No. 9313 ( 2002-04), p. 1207-1209
    In: The Lancet, Elsevier BV, Vol. 359, No. 9313 ( 2002-04), p. 1207-1209
    Type of Medium: Online Resource
    ISSN: 0140-6736
    RVK:
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2002
    detail.hit.zdb_id: 2067452-1
    detail.hit.zdb_id: 3306-6
    detail.hit.zdb_id: 1476593-7
    SSG: 5,21
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