Twort C H, Neild J E, Cameron I R
Clin Sci (Lond). 1985 Sep;69(3):361-4. doi: 10.1042/cs0690361.
Two groups of eight normal subjects were investigated in separate studies to demonstrate the effects of changes in end-tidal PCO2, and of pretreatment with the calcium antagonist drug verapamil, on bronchoconstriction provoked by voluntary hyperventilation. Total respiratory resistance (Ros) was measured by the forced oscillation technique before and after 90 s voluntary hyperventilation. End-tidal PCO2 during hyperventilation was varied by altering inspired CO2 concentration. When end-tidal PCO2 fell during hyperventilation, there was a rise in Ros. This did not occur if end-tidal PCO2 was controlled at a normal resting level during hyperventilation. Specific conductance (sGaw) was measured before and after 90 s voluntary hyperventilation of air. Subjects were treated with oral verapamil or placebo for 2 1/2 days and the effect of hyperventilation on sGaw was reassessed. Verapamil reduced significantly the fall in sGaw caused by hyperventilation. Placebo had no effect. In normal humans, bronchoconstriction provoked by hyperventilating air at ambient temperature and humidity is mediated by the fall in PCO2, and is also reduced by verapamil.
在两项独立研究中，对两组各八名正常受试者进行了调查，以证明呼气末二氧化碳分压（PCO2）的变化以及钙拮抗剂维拉帕米预处理对自愿过度通气诱发的支气管收缩的影响。在90秒自愿过度通气前后，通过强迫振荡技术测量总呼吸阻力（Ros）。通过改变吸入二氧化碳浓度来改变过度通气期间的呼气末PCO2。当过度通气期间呼气末PCO2下降时，Ros会升高。如果在过度通气期间将呼气末PCO2控制在正常静息水平，则不会出现这种情况。在对空气进行90秒自愿过度通气前后测量比气道传导率（sGaw）。受试者口服维拉帕米或安慰剂2.5天，然后重新评估过度通气对sGaw的影响。维拉帕米显著减轻了过度通气引起的sGaw下降。安慰剂没有效果。在正常人体中，在环境温度和湿度下过度通气空气诱发的支气管收缩是由PCO2下降介导的，并且也会被维拉帕米减轻。
