OBJECTIVE: To evaluate the effect of selective electrical stimulation of the tensor veli palatini muscle on upper airway patency. METHODS: Pressure-flow relationships were evaluated, in a feline isolated upper airway preparation, to determine the role of the soft palate musculature on airflow dynamics. The tensor veli palatini muscles were selectively stimulated while monitoring upper airway collapsibility (critical pressure), maximal inspiratory airflow, and the nasal resistance upstream to the flow-limiting site. RESULTS: Tensor veli palatini stimulation resulted (mean +/- SEM) in an increase in maximal inspiratory airflow from 74 +/- 13 mL/s to 93 +/- 18 mL/s (P= .04). The increase in maximal inspiratory airflow was associated with a decrease in critical pressure from -2.3 +/- 1.7 cm H2O to -4.7 +/- 2.7 cm H2O (P= .01) and an increase in nasal resistance from 32.4 +/- 24.3 cm H2O x L(-1) s(-1) to 50.8 +/- 29.7 cm H2O x L(-1) s(-1) (P= .02). CONCLUSIONS: Tensor veli palatini stimulation decreases upper airway collapsibility and is likely an integral component in maintaining airway patency. However, the effects of the isolated tensor veli palatini muscles are less significant than those seen previously with physiologic stimuli such as hypercapnia. These findings suggest that upper airway patency, although contributed to by the tensor veli palatini, requires the coordinated activation of palatopharyngeal muscles to adequately influence upper airway collapsibility.
OBJECTIVE: To evaluate the effect of selective electrical stimulation of the tensor veli palatini muscle on upper airway patency. METHODS: Pressure-flow relationships were evaluated, in a feline isolated upper airway preparation, to determine the role of the soft palate musculature on airflow dynamics. The tensor veli palatini muscles were selectively stimulated while monitoring upper airway collapsibility (critical pressure), maximal inspiratory airflow, and the nasal resistance upstream to the flow-limiting site. RESULTS: Tensor veli palatini stimulation resulted (mean +/- SEM) in an increase in maximal inspiratory airflow from 74 +/- 13 mL/s to 93 +/- 18 mL/s (P= .04). The increase in maximal inspiratory airflow was associated with a decrease in critical pressure from -2.3 +/- 1.7 cm H2O to -4.7 +/- 2.7 cm H2O (P= .01) and an increase in nasal resistance from 32.4 +/- 24.3 cm H2O x L(-1) s(-1) to 50.8 +/- 29.7 cm H2O x L(-1) s(-1) (P= .02). CONCLUSIONS: Tensor veli palatini stimulation decreases upper airway collapsibility and is likely an integral component in maintaining airway patency. However, the effects of the isolated tensor veli palatini muscles are less significant than those seen previously with physiologic stimuli such as hypercapnia. These findings suggest that upper airway patency, although contributed to by the tensor veli palatini, requires the coordinated activation of palatopharyngeal muscles to adequately influence upper airway collapsibility.
Authors: H Pho; A B Hernandez; R S Arias; E B Leitner; S Van Kooten; J P Kirkness; H Schneider; P L Smith; V Y Polotsky; A R Schwartz Journal: J Appl Physiol (1985) Date: 2015-10-15
Authors: Andrew Wellman; Pedro R Genta; Robert L Owens; Bradley A Edwards; Scott A Sands; Stephen H Loring; David P White; Andrew C Jackson; Ole F Pedersen; James P Butler Journal: J Appl Physiol (1985) Date: 2014-10-16
Authors: Thomaz Fleury Curado; Arie Oliven; Luiz U Sennes; Vsevolod Y Polotsky; David Eisele; Alan R Schwartz Journal: Chest Date: 2018-09-14 Impact factor: 9.410