PHARYNGEAL MYOPATHY OF LOADED UPPER AIRWAY IN DOGS WITH SLEEP-APNEA

Recent work indicates that upper airway dilator muscles of individuals with obstructive sleep apnea syndrome (OSAS) demonstrate an increased level of activity during wakefulness compared with normal subjects. I n addition, massive bursts of pharyngeal dilator activity are associat ed with the termination of upper airway occlusive events during sleep. This complex pattern of altered pharyngeal dilator activation is also observed in the English bulldog, an animal model of OSAS. In the pres ent study, it was hypothesized that such alterations in activity level might lead to changes in the structure of pharyngeal muscles in the b ulldog. Full-thickness biopsies were obtained from two pharyngeal dila tor muscles, the sternohyoid (SH) and geniohyoid, as well as a limb mu scle, the anterior tibialis, in bulldogs (n = 5) and control dogs (n = 7). Immunohistochemical analysis of myosin heavy chain expression rev ealed an increased contribution of fast type II myosin heavy-chain fib ers to SH in bulldogs. The bulldog SH also demonstrated increased conn ective tissue content compared with control dogs, consistent with the presence of fibrosis. Both pharyngeal dilators in the bulldog exhibite d an elevated proportion of morphologically abnormal fibers indicative of ongoing or prior injury. No differences in any of the above parame ters were seen between bulldogs and control dogs in the anterior tibia lis limb muscle. We conclude that the chronic load and altered pattern of usage imposed on the upper airway dilators in OSAS lead to myopath ic changes that may ultimately impair the ability of these muscles to maintain pharyngeal patency.