Shinozuka N, Lavoie J P, Martin J G, Bates J H
Meakins-Christie Laboratories, Royal Victoria Hospital, Canada.
J Appl Physiol (1985). 1998 Oct;85(4):1464-70. doi: 10.1152/jappl.1998.85.4.1464.
It is well established that the degree of airway smooth muscle shortening produced by a given dose of bronchial agonist is greatly affected by lung volume. The airways are tethered by parenchymal attachments, the tension of which increases progressively with lung volume, thereby presenting a commensurately increasing hindrance to smooth muscle contraction. Earlier studies (P. F. Dillon, M. O. Aksoy, S. P. Driska, and R. A. Murphy. Science 211: 495-497, 1981) presented evidence that smooth muscle contraction initially involves rapidly cycling cross bridges, which then change to noncycling (latch) bridges. They also suggested that most of the muscle shortening occurs during the early rapid cross-bridge phase. This implies that smooth muscle subject to a given load early in contraction should shorten less than when it is subject to the same load later on. An in vitro study (W. Li and N. L. Stephens. Can. J. Physiol. Pharmacol. 72: 1458-1463, 1994) obtained support for this notion. To test this hypothesis in vivo, we measured the changes in lung impedance at 1 and 6 Hz produced in dogs by a bolus intravenous injection of methacholine when lung volume was increased for 10 s at different times after injection. We found that the changes in mechanics were greatly inhibited, whereas lung volume was elevated. However, when lung volume was returned to its initial level, the lung mechanics continued to change at a rate unaffected by the preceding volume change. We conclude that temporary mechanical inhibition of airway smooth muscle shortening in the normal dog in vivo merely delays an otherwise normal course of contraction.
众所周知，给定剂量的支气管激动剂所产生的气道平滑肌缩短程度会受到肺容积的显著影响。气道通过实质附着而被固定，其张力会随着肺容积的增加而逐渐增大，从而对平滑肌收缩造成相应增加的阻碍。早期研究（P.F.狄龙、M.O.阿克索伊、S.P.德里斯卡和R.A.墨菲。《科学》211: 495 - 497, 1981）提供的证据表明，平滑肌收缩最初涉及快速循环的横桥，随后转变为非循环（闩锁）横桥。他们还提出，大部分肌肉缩短发生在早期快速横桥阶段。这意味着在收缩早期承受给定负荷的平滑肌缩短程度应小于后期承受相同负荷时的缩短程度。一项体外研究（W.李和N.L.斯蒂芬斯。《加拿大生理学与药理学杂志》72: 1458 - 1463, 1994）支持了这一观点。为了在体内验证这一假设，我们在犬静脉注射大剂量乙酰甲胆碱后，于不同时间将肺容积增加10秒，测量了此时在1赫兹和6赫兹下肺阻抗的变化。我们发现，当肺容积升高时，力学变化受到极大抑制。然而，当肺容积恢复到初始水平时，肺力学继续以不受先前容积变化影响的速率发生变化。我们得出结论，在正常犬体内，气道平滑肌缩短的暂时机械抑制仅仅延迟了原本正常的收缩过程。
