EFFECT OF ALTERATIONS IN END-TIDAL 002 TENSION ON FLOW RESISTANCE
EFFECT OF ALTERATIONS IN END-TIDAL 002 TENSION ON FLOW RESISTANCE
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DOI：
10.1152/jappl.1964.19.4.745
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发表时间：
1964-01-01
影响因子：
3.3
通讯作者：
BECKLAKE, MR
中科院分区：
文献类型：
--
作者：
NEWHOUSE, MT;MACKLEM, PT;BECKLAKE, MR
在5名正常受试者中研究了持续自主过度通气时PACO 2对流动阻力和通气肺的机械功的影响。低碳酸血症导致流动阻力持续增加。因此，对于约30升/分钟的分钟容量，与45-50 mm Hg的值相比，PACO 2 20-25 mm Hg时的平均吸气流动阻力大133%，肺通气的平均呼吸功大68%。呼气末压和顺应性不受影响。阿托品和异丙肾上腺素均显著降低气道对低PACO 2水平的反应性，并且一起给予，完全阻断该效应。这些发现可以在很大程度上解释呼吸的氧气消耗增加，以及与自愿（即，低碳酸血症）换气过度。
The effect of PACO2 on flow resistance and on the mechanical work of ventilating the lung was studied in five normal subjects during sustained voluntary hyperventilation. Hypocapnia caused a consistent increase in flow resistance. Thus, for a minute volume of approximately 30 liters/min the mean inspiratory flow resistance was 133% greater and the mean respiratory work of ventilating the lungs 68% greater at PACO2 20-25 mm Hg compared to values at 45-50 mm Hg. End-expiratory pressure and compliance were unaffected. Atropine and isoproterenol each markedly diminished the responsiveness of the airways to low PACO2 levels and, given together, blocked the effect completely. These findings could largely account for the increase in oxygen cost of breathing, and in cardiac output associated with voluntary (i.e., hypocapneic) hyperventilation.