Bates J H, Schuessler T F, Dolman C, Eidelman D H
Meakins-Christie Laboratories, Montreal, Quebec, Canada.
J Appl Physiol (1985). 1997 Jan;82(1):55-62. doi: 10.1152/jappl.1997.82.1.55.
The time course of lung impedance changes after intravenous injection of bronchial agonist have produced significant insights into the mechanisms of bronchoconstriction in the dog (J. H. T. Bates, A.-M. Lauzon, G. S. Dechman, G. N. Maksym, and T. F. Shuessler. J. Appl. Physiol. 76: 616-626, 1994). We studied the time course of acute induced bronchoconstriction in five anesthetized paralyzed open-chest rats injected intravenously with a bolus of methacholine. For the 16 s immediately after injection, we held the lung volume constant while applying small-amplitude flow oscillations at 1.48, 5.45, and 19.69 Hz simultaneously, which provided us with continuous estimates of lung resistance (RL) and elastance (EL) at each frequency. This procedure was repeated at initial lung inflation pressures of 0.2, 0.4, and 0.6 kPa. Both RL and EL increased progressively after methacholine administration; however, the rate of change of EL increased dramatically as frequency was increased, whereas RL remained relatively independent of frequency. We interpret these findings in terms of a three-compartment model of the rat lung, featuring two parallel alveolar compartments feeding into a central airway compartment. Model simulations support the notions that both central airway shunting and regional ventilation inhomogeneity developed to a significant degree in our constricted rats. We also found that the rates of increase in both RL and EL were greatly enhanced as the initial lung inflation pressure was reduced, in accord with the notion that parenchymal tethering is an important mechanism limiting the extent to which airways can narrow when their smooth muscle is stimulated to contract.
静脉注射支气管激动剂后肺阻抗变化的时间进程，为深入了解犬支气管收缩机制提供了重要线索（J. H. T. 贝茨、A.-M. 洛宗、G. S. 德克曼、G. N. 马克西姆和T. F. 舒斯勒。《应用生理学杂志》76: 616 - 626, 1994）。我们研究了五只麻醉、麻痹、开胸大鼠静脉注射大剂量乙酰甲胆碱后急性诱导支气管收缩的时间进程。在注射后的16秒内，我们保持肺容积恒定，同时在1.48、5.45和19.69赫兹施加小幅度流量振荡，这使我们能够连续估计每个频率下的肺阻力（RL）和弹性（EL）。在初始肺充气压力为0.2、0.4和0.6千帕时重复此过程。乙酰甲胆碱给药后，RL和EL均逐渐增加；然而，随着频率增加，EL的变化率急剧增加，而RL相对与频率无关。我们根据大鼠肺的三室模型来解释这些发现，该模型的特点是有两个平行的肺泡室通向一个中央气道室。模型模拟支持了这样的观点，即在我们的收缩大鼠中，中央气道分流和区域通气不均匀性都在很大程度上发展。我们还发现，随着初始肺充气压力降低，RL和EL的增加速率都大大提高，这与实质束缚是一种重要机制的观点一致，即当气道平滑肌被刺激收缩时，实质束缚限制了气道变窄的程度。
