Lutchen K R, Greenstein J L, Suki B
Department Biomedical Engineering, Boston University, Massachusetts 02215, USA.
J Appl Physiol (1985). 1996 May;80(5):1696-707. doi: 10.1152/jappl.1996.80.5.1696.
It has been proposed that during mild-to-moderate bronchoconstriction one can partition airway and tissue properties on the basis of input impedance (Zin) acquired from 0.1 to 5 Hz (K.R. Lutchen, B. Suki, Q. Zhang, F. Peták, B. Daróczy, and Z. Hantos. J. Appl. Physiol. 77: 373-385, 1994). The approach is to apply a homogeneous lung model that contains airway resistance and viscoelastic tissue damping and elastance parameters. The tissue parameters account for the frequency dependence in lung resistance (RL) and elastance (EL). We present an anatomically consistent asymmetrically branching airway model to address two key questions: 1) How will lung inhomogeneities, airway wall shunting, and tissue viscoelasticity contribute to increased frequency dependence and levels of RL and EL during lung constriction? and 2) How much can lung inhomogeneities and airway wall shunting contribute to our assessment of airway, tissue, and overall lung properties derived from Zin? The model incorporates nonrigid airway walls and allows for explicit control over the type and degree of inhomogeneous airway constriction or tissue changes. Our results indicate that, from 0.1 to 5 Hz, airway wall shunting does not become important unless the entire lung periphery experiences significant constriction. Mild-to-moderate inhomogeneous peripheral airway constriction produces a relatively minor additional frequency dependence in RL and EL beyond that due to the tissues alone. With more extreme constriction, however, there is a marked frequency-dependent increase in EL. This phenomenon may render it impossible to distinguish from a single frequency measurement whether an increase in EL during bronchoconstriction is a consequence of a true increase in tissue stiffening or simply a consequence of airway phenomena. Finally, Zin from 0.1 to 5 Hz can be used to provide a reasonable separation of airway and tissue properties for mild-to-moderate homogeneous or inhomogeneous lung constriction. However, during more severe disease, inhomogeneities and/or wall shunting will produce substantial overestimation of tissue damping and hysteretic properties. In fact, the only reliable indicator of a real change in the tissues may be a change in the estimate of tissue elastance that is based on data extending to a sufficiently low frequency.
有人提出,在轻度至中度支气管收缩期间,可以根据从0.1至5赫兹获取的输入阻抗(Zin)来区分气道和组织特性(K.R.卢琴、B.苏基、Q.张、F.佩塔克、B.达罗奇和Z.汉托斯。《应用生理学杂志》77: 373 - 385, 1994)。该方法是应用一个包含气道阻力以及粘弹性组织阻尼和弹性参数的均匀肺模型。组织参数说明了肺阻力(RL)和弹性(EL)中的频率依赖性。我们提出一个解剖学上一致的不对称分支气道模型来解决两个关键问题:1)肺的不均匀性、气道壁分流以及组织粘弹性在肺收缩期间如何导致频率依赖性增加以及RL和EL水平升高?2)肺的不均匀性和气道壁分流在多大程度上会影响我们从Zin得出的对气道、组织和整体肺特性的评估?该模型纳入了非刚性气道壁,并允许对不均匀气道收缩或组织变化的类型和程度进行明确控制。我们的结果表明,在0.1至5赫兹范围内,除非整个肺周边都经历显著收缩,气道壁分流才会变得重要。轻度至中度的不均匀周边气道收缩在RL和EL中产生的额外频率依赖性相对较小,超出了仅由组织导致的频率依赖性。然而,在更极端的收缩情况下,EL会有明显的频率依赖性增加。这种现象可能使得从单一频率测量中无法区分支气管收缩期间EL的增加是组织真正变硬的结果还是仅仅是气道现象的结果。最后,对于轻度至中度的均匀或不均匀肺收缩,0.1至5赫兹的Zin可用于合理区分气道和组织特性。然而,在更严重的疾病中,不均匀性和/或壁分流会导致对组织阻尼和滞后特性的大幅高估。实际上,组织真正变化的唯一可靠指标可能是基于延伸到足够低频率的数据得出的组织弹性估计值的变化。