Gelb Arthur F, Taylor Colleen Flynn, Cassino Cara, Shinar Chris M, Schein Mark J, Zamel Noe
Pulmonary Division, Department of Medicine, Lakewood Regional Medical Center, Lakewood, CA, USA.
Pulm Pharmacol Ther. 2009 Jun;22(3):237-42. doi: 10.1016/j.pupt.2008.12.018. Epub 2009 Jan 3.
The magnitude of tiotropium (1) induced bronchodilation and (2) protection against dynamic hyperinflation in COPD phenotypes has not been studied.
We studied moderate to severe COPD patients with varying extent of emphysema as evaluated by high-resolution thin-section lung CT. Spirometry including inspiratory capacity (IC) was measured before and immediately after metronome paced hyperventilation (MPH) at 2 times resting respiratory rate for 20s to induce dynamic hyperinflation. Spirometry was obtained at baseline and pre- and 1.5h post-18 microg tiotropium via HandiHaler after 30 day tiotropium treatment period in a single blind, open label intervention.
In 29 COPD patients (15M), age 70+/-9 years (mean+/-SD) with smoking history of 53+/-37 pack years, baseline forced expiratory volume in 1s (FEV(1)) post-180 microg albuterol MDI was 1.6+/-0.4 L (61+/-8% predicted) and FEV(1)/FVC 59+/-6%. Lung CT emphysema score (LCTES) was 23+/-20 (mean+/-SD) on a scale of 0-100 (none to most severe emphysema). After 30-day tiotropium, FEV(1) increased 101+/-124 mL (mean+/-SD) (p<0.001) and Spearman correlation (r)=-0.04, p=0.8 with LCTES; IC increased 163+/-232 mL (p<0.001), and r=-0.2, p=0.3 with LCTES. Results following MPH induced DH before and after 30-day tiotropium were significant (p<0.001) and similar: IC decreased 340+/-280 mL before and 337+/-270 mL after tiotropium, and r=-0.3, p=0.9 with LCTES.
Tiotropium significantly increased FEV(1) (L) and inspiratory capacity in moderate-severe COPD, independent of extent of lung CT emphysema score. Despite bronchodilation and lower resting lung volume, tiotropium did not abbreviate induced dynamic hyperinflation, which was also independent of underlying emphysema.
噻托溴铵（1）诱导的支气管扩张程度以及（2）对慢性阻塞性肺疾病（COPD）不同表型动态肺过度充气的保护作用尚未得到研究。
我们研究了通过高分辨率薄层肺部CT评估的、肺气肿程度不同的中重度COPD患者。在以两倍静息呼吸频率进行节拍器控制的过度通气（MPH）20秒以诱导动态肺过度充气之前和之后，立即测量包括吸气容量（IC）在内的肺功能。在为期30天的噻托溴铵治疗期后，通过HandiHaler给予18微克噻托溴铵，在基线以及给药前和给药后1.5小时进行单盲、开放标签干预下的肺功能测量。
29例COPD患者（15例男性），年龄70±9岁（均值±标准差），吸烟史53±37包年，在吸入180微克沙丁胺醇MDI后，基线1秒用力呼气容积（FEV₁）为1.6±0.4升（预测值的61±8%），FEV₁/FVC为59±6%。肺部CT肺气肿评分（LCTES）在0 - 100分（无肺气肿至最严重肺气肿）范围内为23±20（均值±标准差）。30天噻托溴铵治疗后，FEV₁增加101±124毫升（均值±标准差）（p<0.001），与LCTES的Spearman相关性（r）=-0.04，p = 0.8；IC增加163±232毫升（p<0.001），与LCTES的r=-0.2，p = 0.3。30天噻托溴铵治疗前后MPH诱导的动态肺过度充气后的结果具有显著性（p<0.001）且相似：噻托溴铵治疗前IC降低340±280毫升，治疗后降低337±270毫升，与LCTES的r=-0.3，p = 0.9。
噻托溴铵显著增加中重度COPD患者的FEV₁（升）和吸气容量，与肺部CT肺气肿评分程度无关。尽管有支气管扩张和较低的静息肺容积，但噻托溴铵并未缩短诱导的动态肺过度充气，这也与潜在的肺气肿无关。
