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Effects of hypercapnia and hypocapnia on respiratory resistance in normal and asthmatic subjects.

机译:高碳酸血症和低碳酸血症对正常和哮喘患者呼吸抵抗的影响。

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摘要

The effects of hypercapnia and hypocapnia on respiratory resistance were studied in 15 healthy subjects and 30 asthmatic subjects. Respiratory resistance (impedance) was measured with the pseudo-random noise forced oscillation technique while the subjects rebreathed from a wet spirometer in a closed respiratory circuit in which end tidal carbon dioxide tension (PCO2) could be controlled. Hypercapnia was induced by partially short circuiting the carbon dioxide absorber, and hypocapnia by voluntary hyperventilation. The circulating air was saturated with water vapour and kept at body temperature and ambient pressure. A rise of end tidal PCO2 of 1 kPa caused a significant fall in respiratory resistance in both normal and asthmatic subjects (15% and 9% respectively). A fall of PCO2 of 1 kPa did not cause any significant change in impedance in the control group. In the asthmatic patients resistance increased by 13%, reactance fell by 45%, and the frequency dependence of resistance rose 240%. These findings confirm that hypocapnia may contribute to airway obstruction in asthmatic patients, even when water and heat loss are prevented.
机译:在15名健康受试者和30名哮喘受试者中研究了高碳酸血症和低碳酸血症对呼吸阻力的影响。使用伪随机噪声强制振荡技术测量呼吸阻力(阻抗),而受试者在闭合呼吸回路中从湿式肺活量计呼吸,可控制最终的潮气二氧化碳张力(PCO2)。高碳酸血症是通过二氧化碳吸收器的部分短路引起的,而高碳酸血症是通过自愿过度换气引起的。循环空气中充满水蒸气,并保持在体温和环境压力下。潮气末PCO2升高1 kPa会使正常人和哮喘患者的呼吸阻力显着下降(分别为15%和9%)。 PCO2下降1 kPa并不会在对照组中引起任何明显的阻抗变化。在哮喘患者中,耐药性增加了13%,电抗下降了45%,耐药性的频率依赖性上升了240%。这些发现证实,即使预防水和热量流失,低碳酸血症也可能导致哮喘患者的气道阻塞。

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