Glottic closing force in an anesthetized, awake pig model: biomechanical effects on the laryngeal closure reflex resulting from altered central facilitation.

Reflex sphincteric closure of the larynx, essential to lower airway protection, is most efficiently achieved through strong reflex adduction by both vocal cords. Because the conversion of a bilaterally evoked response to a unilaterally evoked one appears anesthesia-dependent, we hypothesized that central facilitation is an essential component of a bilateral adductor reflex and that its disturbance could result in weakened sphincteric closure. Six adult 50 kg pigs were used in this study. During electrical stimulation of the internal branch of the superior laryngeal nerve (iSLN) using bipolar platinum-iridium electrodes, the force of the evoked glottic closure response was measured using a pressure transducer positioned between both vocal cords, while electromyographic evoked response was recorded from both thyroarytenoid muscles under varying levels [0.5-1.0 minimal alveolar concentration (MAC)] of isoflurane anesthesia. The force of glottic closure appeared less under deep anesthesia, even with bilateral stimulation of the iSLN, than under light anesthesia with unilateral stimulation. As anesthetic levels approached 1.0 MAC, the glottic closing force decreased to 52-72% of the force measured under 0.5 MAC light anesthesia. Although it is generally understood that alteration of central facilitation by deepening anesthesia abolishes the crossed adductor reflex, the biomechanical effects of altered central facilitation on force differentials have never been previously demonstrated. Precise understanding of this effect may improve the prevention of aspiration in patients emerging from heavy sedation or under prolonged psychotropic control.