Invited editorial on "Neuromechanical interaction in human snoring and upper airway obstruction".
Invited editorial on "Neuromechanical interaction in human snoring and upper airway obstruction".
复制标题
“人类打鼾和上呼吸道阻塞中的神经机械相互作用”特邀社论。
DOI:
10.1152/jappl.1999.86.6.1757
复制
发表时间:
1999
期刊:
影响因子:
--
通讯作者:
Roberts,D
中科院分区:
文献类型:
--
作者:
Roberts,D
IN THIS ISSUE of the Journal, Huang and Ffowcs Williams (3) report the development of a mathematical model that couples flow mechanics of the upper airway with neurophysiological activity. The model depends on the mechanical principle that luminal collapse occurs when passive wall stiffness is insufficient to withstand falling intraluminal pressure and on the physiological principle that proprioception in the collapsing wall triggers reflex muscle activity in ‘‘dilator’’muscles that increases the ‘‘neural’’stiffness of the wall and prevents collapse from continuing. The model shows that, in this situation, reflex latency is a critical factor because, if the latency is larger than an optimal value, part of the neuromuscular force is transformed into a negative damping effect that destabilizes the luminal wall and results in ‘‘flutter.’’Mathematical modeling is not a new approach to understanding the function of the airway; Isono and colleagues (4, 5) showed that the mechanics of flow through an airway with passive, compliant walls can result directly in luminal collapse; the critical factors are the morphology of the lumen and the rate of flow. As it is generally understood that during rapid-eyemovement (REM) sleep the active components of wall compliance are negated as a result of muscle inactivity, the mechanical conditions of these models are closely approximated during deep sleep. Isono et al.(5) subsequently showed that the morphologies of airways rendered passive in vivo do, indeed, differ significantly between apneic and normal subjects. In the awake subject, when luminal volume and axial bending, and combined passive and active wall stiffness, are compared, the morphological values for the airway in apneic subjects with low apnea/hypopnea indexes overlap considerably those of subjects with normal airways (unpublished observations). This shows that a functional lumen is maintained during wakefulness and in the pre-REM phases of sleep through the agency of neurological activity that increases the active component of wall compliance, ie, via dilator muscle activity. Presumably, with the onset of REM sleep and cessation of muscle reflex activity, the overlapping morphologies would be altered sufficiently to become distinct groups. Horner et al.(2) showed that the genioglossus muscle is active during the early phases of sleep and is more active in apneic than in nonapneic airways. This implies that greater neuromuscular effort is required to maintain functional viability in airways that are prone to collapse than in airways that are not prone to collapse. In terms of the Huang and Ffowcs Williams model, the struggle to maintain airway viability can be seen as a progressive destabilization of the lumen wall caused by dilator muscle reflexes unable to match the rapid onset of collapse. However, a neuromechanical coupling model also presents the possibility that the problem may be inherent tardiness in the reflex itself, ie, within the integrative pathways in the brain stem. These alternatives, and the significance of neuromechanical coupling, can be understood in the context of phylogenetic modifications of the human airway.The high incidence of snoring and obstructive sleep apnea (3) suggests that the human airway is not optimally adapted to its prime function. However, the airway is a special case and has been extensively modified by adaptive forces not related to its original and prime functions. It is generally accepted that these adaptations relate to a whole body change from a pronograde to a unique orthograde posture. They included extensive bony remodeling of the skull. The facial skeleton rotated beneath the rostral portion of the cranium while …
登录
查看更多内容
DOI:
10.1164/arrd.1984.130.4.588
发表时间:
2015-05
期刊:
The American review of respiratory disease
影响因子:
--
作者:
M. Sackner;H. Gonzalez;M. Rodríguez;A. Belsito;D. R. Sackner;S. Grenvik
通讯作者:
M. Sackner;H. Gonzalez;M. Rodríguez;A. Belsito;D. R. Sackner;S. Grenvik
影响因子:
5.2
作者:
I. Hodges;R. C. Groggins;A. Milner;G. M. Stokes
通讯作者:
G. M. Stokes
DOI:
10.1172/jci103441
发表时间:
1957
期刊:
The Journal of clinical investigation
影响因子:
--
作者:
C. Cook;J. Sutherland;S. Segal;R. B. Cherry;J. Mead;M. Mcilroy;C. Smith
通讯作者:
C. Smith
DOI:
--
发表时间:
1985
期刊:
American Review of Respiratory Disease
影响因子:
--
作者:
David R. Hillman;L. Prentice;Kevin E. Finucane
通讯作者:
Kevin E. Finucane
DOI:
--
发表时间:
2015
期刊:
American Review of Respiratory Disease
影响因子:
--
作者:
J. Sharp;N. B. Goldberg;W. Druz;H. Fishman;J. Danon
通讯作者:
J. Danon