van den Elshout F J, van Herwaarden C L, Folgering H T
Department of Pulmonary Diseases, University of Nijmegen, Groesbeek, The Netherlands.
Thorax. 1991 Jan;46(1):28-32. doi: 10.1136/thx.46.1.28.
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.
在15名健康受试者和30名哮喘患者中研究了高碳酸血症和低碳酸血症对呼吸阻力的影响。采用伪随机噪声强迫振荡技术测量呼吸阻力(阻抗),同时受试者在封闭呼吸回路中从湿肺量计进行重复呼吸,其中终末潮气二氧化碳分压(PCO2)可得到控制。通过使二氧化碳吸收器部分短路诱导高碳酸血症,通过自主过度通气诱导低碳酸血症。循环空气用水蒸气饱和,并保持在体温和环境压力下。终末潮气PCO2升高1 kPa导致正常受试者和哮喘患者的呼吸阻力均显著下降(分别为15%和9%)。PCO2下降1 kPa在对照组中未引起阻抗的任何显著变化。在哮喘患者中,阻力增加了13%,电抗下降了45%,阻力的频率依赖性增加了240%。这些发现证实,即使在防止水分和热量流失的情况下,低碳酸血症也可能导致哮喘患者气道阻塞。