Gorman R B, McKenzie D K, Gandevia S C, Plassman B L
Department of Respiratory Medicine, Prince Henry Hospital, NSW, Sydney, Australia.
Thorax. 1992 Nov;47(11):922-7. doi: 10.1136/thx.47.11.922.
This study investigated whether the inspiratory muscles are susceptible to fatigue during acute airway narrowing because of increased airway resistance and hyperinflation.
Asthmatic subjects performed up to four series (on separate days) of 18 maximal static inspiratory efforts of 10 seconds' duration with 10 second rest intervals (50% duty cycle; total duration six minutes): at functional residual capacity (FRC) (control); after histamine induced bronchoconstriction, which decreased forced expiratory volume in one second (FEV1) to a mean of 55% (SD 11%) of the initial value; at a voluntarily increased lung volume (initial volume held at 140% control); and after inhalation of histamine at a voluntarily increased lung volume.
For the group of subjects the mean (SD) maximal inspiratory pressure (MIP) in the control experiments was 114 (22) cmH2O and the initial volume was 3.5 (1.2) 1. After histamine inhalation the initial lung volume for contractions increased to 118% (5%) of the control volume. In the high lung volume experiments initial volumes were 140% (12%) of the control (volume without histamine) and 140% (15%) (with histamine). The relation between MIP and initial absolute lung volume was determined for each subject before fatigue developed. When the inspiratory pressures for each contraction in the endurance test were normalised to the pressure expected for that lung volume, no significant differences were found between the four experimental conditions for MIP, or between pressures sustained over the 18 contractions.
Histamine induced bronchoconstriction and hyperinflation had no detectable effect on inspiratory muscle strength or endurance in these asthmatic subjects.
本研究调查了在急性气道狭窄期间，由于气道阻力增加和肺过度充气，吸气肌是否易疲劳。
哮喘患者（在不同日期）进行多达四组，每组18次持续10秒的最大静态吸气动作，每次动作间休息10秒（占空比50%；总时长6分钟）：在功能残气量（FRC）时（对照）；在组胺诱导支气管收缩后，此时一秒用力呼气量（FEV1）降至初始值的平均55%（标准差11%）；在自主增加肺容积时（初始容积保持在对照值的140%）；以及在自主增加肺容积时吸入组胺后。
对于该组受试者，对照实验中的平均（标准差）最大吸气压力（MIP）为114（22）cmH₂O，初始容积为3.5（1.2）升。吸入组胺后，收缩时的初始肺容积增加至对照容积的118%（5%）。在高肺容积实验中，初始容积为对照（无组胺时的容积）的140%（12%）以及（有组胺时）的140%（15%）。在疲劳出现前，为每个受试者确定MIP与初始绝对肺容积之间的关系。当将耐力测试中每次收缩的吸气压力标准化为该肺容积预期的压力时，在四种实验条件下，MIP之间或18次收缩中持续的压力之间均未发现显著差异。
组胺诱导的支气管收缩和肺过度充气对这些哮喘患者的吸气肌力量或耐力没有可检测到的影响。
