Mortola J P, Milic-Emili J, Noworaj A, Smith B, Fox G, Weeks S
Am Rev Respir Dis. 1984 Jan;129(1):49-53. doi: 10.1164/arrd.1984.129.1.49.
The postinspiratory activity of the inspiratory muscles (Pmusl) was estimated in 12 infants (2 to 4 days old) by analysis of the rise in mask pressure after airway occlusion at end inspiration. We reasoned that if at the end of inspiration Pmusl instantaneously ceased, the mask pressure would immediately increase to the relaxation pressure value corresponding to that volume. Any delay would suggest some degree of Pmusl. In 9 infants, Pmusl reached zero before the end of an average expiration (TE), although lasting for a long portion of TE (83% +/- 25 SD). We then compared the expiratory tidal flow-volume curves during resting breathing with the curves of "relaxed" expirations. In general, the tidal curve shows a linear portion that can be extrapolated to zero flow. From this extrapolation it is apparent that the end-expiratory level (FRC) is above the resting volume of the respiratory system (Vr), the FRC-Vr difference averaging 3.11 ml/kg. In 6 infants, the tidal expiratory flow-volume curve was displaced to the left of the "relaxed" curve, whereas in the remaining infants the two curves superimposed. These analyses suggest that in infants during tidal breathing (1) Pmusl can substantially contribute to the rise in FRC, and (2) the final portion of expiration is in most cases "relaxed." In some infants, however, a braking mechanism, probably of laryngeal origin, further decreases the expiratory flow and may contribute in maintaining the mean lung volume elevated.
通过分析吸气末气道阻塞后面罩压力的升高情况,对12名2至4日龄婴儿的吸气肌吸气后活动(Pmusl)进行了评估。我们推断,如果在吸气末Pmusl瞬间停止,面罩压力将立即升至与该容积相对应的松弛压力值。任何延迟都表明存在一定程度的Pmusl。在9名婴儿中,Pmusl在平均呼气(TE)结束前降至零,尽管在TE的很长一段时间内持续存在(83%±25标准差)。然后,我们将静息呼吸时的呼气潮气量-流速曲线与“松弛”呼气曲线进行了比较。一般来说,潮气量曲线有一个可外推至零流速的线性部分。从这种外推可以明显看出,呼气末水平(FRC)高于呼吸系统的静息容积(Vr),FRC与Vr的差值平均为3.11 ml/kg。在6名婴儿中,潮气量呼气量-流速曲线向左偏离“松弛”曲线,而在其余婴儿中,两条曲线重叠。这些分析表明,在婴儿潮式呼吸过程中:(1)Pmusl可显著促进FRC的升高;(2)在大多数情况下,呼气的最后部分是“松弛的”。然而,在一些婴儿中,一种可能源于喉部的制动机制会进一步降低呼气流量,并可能有助于维持平均肺容积升高。