Modulation of myosin heavy chains in rat laryngeal muscle

• Published in: The Laryngoscope Vol. 111; no. 3; p. 472
• Main Authors: Shiotani, A, Nakagawa, H, Flint, P W
• Format: Journal Article
• Language: English
• Published: United States 01.03.2001
• Subjects: Animals; Electromyography; Microsurgery; Myosin Heavy Chains - metabolism; Nerve Regeneration - physiology; Rats; Rats, Sprague-Dawley; Recurrent Laryngeal Nerve - pathology; Recurrent Laryngeal Nerve - surgery; Recurrent Laryngeal Nerve Injuries; Vocal Cords - innervation; Vocal Cords - pathology; Vocal Cords - physiopathology; Vocalization, Animal - physiology
• ISSN: 0023-852X
• DOI: 10.1097/00005537-200103000-00017

To test the hypothesis that myosin heavy chain (MHC) composition is a biological marker indicative of appropriate and functional reinnervation. Age-matched adult rats were randomized for prospective study under three experimental conditions. In adult rats, three experimental conditions were surgically created, including transient recurrent laryngeal nerve (RLN) crush injury, RLN transection and repair, and cricoarytenoid joint fixation with intact RLN. Animals were survived for 30, 90, and 180 days. At each interval, vocal fold mobility was assessed by rigid microlaryngoscopy. Laryngeal electromyography (EMG) was performed before euthanasia. The thyroarytenoid and posterior cricoarytenoid muscles were then excised, each muscle was processed for sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and MHC composition was determined. Thirty days after nerve crush injury, three of six animals regained vocal fold mobility and normal MHC composition. Impaired vocal fold motion in three of six animals was associated with MHC composition characteristic of denervation. At 90 and 180 days, normal vocal fold motion and normal MHC composition were observed in all animals. Following nerve transection and repair, impaired vocal fold motion and MHC composition characteristic of denervation were observed in all animals, despite evidence of reinnervation on EMG. Following joint fixation, alteration in MHC composition consistent with denervation was observed only at 30 days, as was evident in the nerve crush model. Temporary injury and vocal fold immobilization result in transient shifts in MHC composition. Nerve transection and repair result in persistent alteration of MHC composition and vocal fold dysfunction. The expression of normal MHC composition is dependent on the condition of appropriate neural contact and functional reinnervation.