摘要
我们研究了11例轻度哮喘患者,以验证是否可以通过被动改变肺容积来抑制或克服哮喘的恶性膨胀机制。第1天,我们通过吸入甲胆碱诱导1秒内用力呼气量(FEV1)下降30-60%,并测量FRC (delta FRC)的增加。δ FRC为729 +/- 378 ml(均值+/- SD)。第2天,受试者仰卧在铁肺内,测量食管(Poes)、胃(Pgas)和经膈(Pdi)压力,以及在支气管刺激前后由胸外压力引起的功能剩余容量(FRC) (delta V)的变化。在正压力下,FRC下降,在10cmh2o或更高的压力下达到平台。在支气管刺激后,该平台的平均FRC比之前高839 ml。FRC的Pdi与胸外压力的变化方向一致,且不受支气管痉挛的影响。在铁肺不施加压力的情况下,甲胆碱后吸气峰值Pdi由13.6 +/- 5.4上升至28.1 +/- 13.5 cmH2O;- 20cmh2o胸外压降低后者为15.4 +/- 7.3 cmH2O (p < 0.01)。刺激后肺容积的增加和胸壁反冲曲线的移位不受胸外正压或负压的抑制。 Our data show that the mechanisms of hyperinflation are not eliminated or overcome by passively changing lung volumes and support the hypothesis that persisting activity of inspiratory muscles other than the diaphragm during expiration and perhaps a prolonged expiratory time constant are responsible for hyperinflation in asthma.