文摘
Summary
Failure to maintain the patency of the pharyngeal airway during sleep is central to the pathogenesis of obstructive sleep apnoea (OSA). This failure is hypothesised to be due to the combination of a small pharyngeal airway and inadequate state-dependent neuro-mechanical control. Little is known of how the pharyngeal muscles function in an integrated function to alter the size and shape of the pharyngeal airway. We hypothesise that the muscles of the pharynx function as a muscular hydrostat. Muscular hydrostats are organs that are composed almost entirely of muscle, with a complex muscular arrangement within the organ. Examples of muscular hydrostats include the mammalian tongue, octopus tentacles, elephant trunks and the medicinal leech. During muscle contraction the organ will maintain a constant volume as muscle tissue is mostly water and hence incompressible. The mechanical effect of contraction of individual muscles within the muscular hydrostat is dependent on the integrated activity of all other muscles, as muscle orientation is dependent on the organ shape. Functionally the significance of the muscular hydrostat model lies in the concept that alterations in organ shape are achieved via muscle contraction driven redistribution of hydrostatic tissue pressure. The tissues which comprise the pharynx are predominantly muscle, and thus incompressible. The pharynx is composed of 20 muscles that are arranged in a complex fashion. Within the peri-pharyngeal tissues the only bony structure is the hyoid bone and in adult humans this is a free-floating bone. Evidence already exists that the functional outcome of contraction of some of the pharyngeal muscles is dependent on stage of respiration, the intra-luminal pressure, or the position of the hyoid bone when the muscle is activated. There is also evidence that muscle contraction can alter the pressure in the tissues surrounding the pharynx in a non-uniform fashion. However, it has not been demonstrated for the pharynx that pharyngeal luminal shape is determined by muscle contraction determined transmural pressure distribution. The consequences of this hypothesis are that reported pharyngeal anatomical abnormalities in subjects with OSA, such as increased peri-pharyngeal fat deposition or thickening of the lateral pharyngeal walls, could result in alteration in integrated muscular function and thus a failure to maintain upper airway patency. In addition, nocturnal pharyngeal airway obstruction may result from a failure of cross muscle activation. This novel paradigm may lead to greater insights into the pathogenesis of OSA as well as opening new avenues for exploration of novel therapeutic strategies.
