Pulmonary mechanics and gas exchange in seated normal men with chest restriction.
Pulmonary mechanics and gas exchange in seated normal men with chest restriction.
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胸部受限的正常坐位男性的肺力学和气体交换。
DOI：
10.1152/jappl.1981.51.1.26
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发表时间：
1981
期刊：
影响因子：
--
通讯作者：
Hyatt,RE
中科院分区：
文献类型：
--
作者：
Klineberg,PL;Rehder,K;Hyatt,RE
本文测定了正常坐位正常人在行带前、呼吸空气(CAIR)和带胸呼吸空气(SAIR)或100%氧气(SO2)时的肺容量、静态压力-容量曲线、最大呼气流量-容量曲线、右向左肺内分流(Qs/Qt)、肺泡通气量/灌注率(VA/Q)的分布。使用Sair和SO2后，平均肺活量比对照组减少了44%。总肺活量(TLC)由4.64+/-0.39cmH2O(平均值+/-SE)增加到7.00+/-0.47cmH2O，SO2组增加到7.24+/-0.70cmH2O(P<0.05)。对照组TLC 50%处最大呼气流量显著增加(P<0.05)，由3.22增至0.25 L/S(均值+/-SE)至5.84+/-0.69 L/S及5.50+/-0.68 L/S(P<0.05)。使用Sair时，Qs/Qt与对照组相比没有显著增加。加入SO2后，平均Qs/Qt显著增加(P<0.05)，从心输出量的0增加到2.2+/-0.9%。因此，肺不张的发展，如Qs/Qt的增加，不太可能是Sair和SO2引起的PST(L)增加的原因。目前的证据表明，无论是肺泡表面顺应性的改变还是肺的扭曲，或者两者兼而有之，都是导致反冲压力增加的原因，但似乎没有哪一种机制能完全解释这一点。
Lung volumes, static pressure-volume curves, maximal expiratory flow-volume curves, right-to-left intrapulmonary shunts (Qs/Qt), and distributions of ventilation and perfusion relative to the alveolar ventilation and perfusion ration (VA/Q) were determined in seated normal men before chest strapping while breathing air (Cair) and during chest strapping while breathing air (Sair) or 100% oxygen (So2). With Sair and So2, mean vital capacity was reduced by 44% from control. Elastic recoil pressure [Pst(L)] of the lung at 50% control total lung capacity (TLC) increased significantly (P less than 0.05) from 4.64 +/- 0.39 cmH2O (mean +/- SE) to 7.00 +/- 0.47 cmH2O with Sair and to 7.24 +/- 0.70 cmH2O with So2. Maximal expiratory flow at 50% of control TLC increased significantly (P less than 0.05) from 3.22 to 0.25 l/s (mean +/- SE) to 5.84 +/- 0.69 l/s with Sair and to 5.50 +/- 0.68 l/s with So2. With Sair, no significant increase in Qs/Qt from control was observed. With So2, mean Qs/Qt increased significantly (P less than 0.05) from 0 to 2.2 +/- 0.9% of the cardiac output. It is therefore unlikely that the development of atelectasis, as indicated by an increase in Qs/Qt, accounts for the increase in Pst (L) with Sair and So2. Current evidence suggests that either change in alveolar surface compliance or distortion of the lung or both are responsible for the increased recoil pressure but that neither mechanism alone appears to explain it totally.