Invited editorial on "Neuromechanical interaction in human snoring and upper airway obstruction".

Invited editorial on "Neuromechanical interaction in human snoring and upper airway obstruction".
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“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
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发表时间:
1999
期刊:
Journal of applied physiology (Bethesda, Md. : 1985)
影响因子:
--
通讯作者:
Roberts,D
Roberts,D
中科院分区:
--
文献类型:
--
作者:
Roberts,D

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在本期杂志中,Huang和Ffowcs威廉姆斯(3)报告了一个数学模型的发展,该模型将上气道的流动力学与神经生理活动相结合。该模型依赖于机械原理,即当被动壁刚度不足以承受下降的管腔内压力时发生管腔塌陷,以及生理原理,即塌陷壁中的本体感受触发“扩张器”肌肉中的反射性肌肉活动,从而增加壁的“神经”刚度并防止塌陷继续。该模型表明,在这种情况下,反射潜伏期是一个关键因素,因为如果潜伏期大于最佳值,部分神经肌肉力将转化为负阻尼效应,使管腔壁不稳定并导致“颤动”。数学建模并不是理解气道功能的新方法; Isono及其同事(4,5)表明,通过具有被动顺应性壁的气道的流动力学可直接导致管腔塌陷;关键因素是管腔的形态和流速。由于通常理解的是,在快速眼动(REM)睡眠期间,由于肌肉不活动,壁顺应性的活动分量被否定,这些模型的机械条件在深度睡眠期间非常接近。Isono等人(5)随后表明,在呼吸暂停和正常受试者之间,在体内呈现被动的气道的形态确实显著不同。在清醒受试者中,当比较管腔容积和轴向弯曲以及被动和主动壁刚度时,低呼吸暂停/呼吸不足指数的呼吸暂停受试者的气道形态值与正常气道受试者的气道形态值相当重叠(未发表的观察结果)。这表明,在清醒期间和睡眠的REM前阶段,通过神经活动的代理,即通过扩张肌活动,增加壁顺应性的活性成分,维持功能性管腔。据推测,随着快速眼动睡眠的开始和肌肉反射活动的停止,重叠的形态将发生充分的改变,成为不同的群体。Horner等人(2)显示颏舌肌在睡眠的早期阶段是活跃的,并且在呼吸暂停的气道中比在非呼吸暂停的气道中更活跃。这意味着在易于塌陷的气道中比在不易塌陷的气道中需要更大的神经肌肉努力来维持功能存活力。根据Huang和Ffowcs威廉姆斯模型,维持气道活力的努力可以被视为由扩张肌反射无法匹配塌陷的快速发生引起的管腔壁的进行性不稳定。然而,神经机械耦合模型也提出了一种可能性,即问题可能是反射本身固有的迟缓,即脑干中的整合通路。这些替代方案以及神经机械耦合的重要性可以在人类气道系统发育修饰的背景下理解。打鼾和阻塞性睡眠呼吸暂停的高发病率表明人类气道没有最佳地适应其主要功能。然而,气道是一个特殊的情况,并已被广泛修改的自适应力不相关的原始和主要功能。人们普遍认为,这些适应性变化与整个身体从前倾到独特的直立姿势的变化有关。包括头骨的大面积骨重塑。面部骨骼在头盖骨的喙部下方旋转,同时...
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 …
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