O'Donnell Denis E, Hamilton Alan L, Webb Katherine A
Department of Medicine, Respiratory Investigation Unit, Queen's University, Kingston, Ontario, Canada.
J Appl Physiol (1985). 2006 Oct;101(4):1025-35. doi: 10.1152/japplphysiol.01470.2005. Epub 2006 May 4.
During constant-work-rate exercise in chronic obstructive pulmonary disease, dyspnea increases steeply once inspiratory reserve volume (IRV) falls to a critical level that prevents further expansion of tidal volume (Vt). We studied the effects of this mechanical restriction on the quality and intensity of exertional dyspnea and examined the impact of an anticholinergic bronchodilator. In a randomized, double-blind, crossover study, 18 patients with chronic obstructive pulmonary disease (forced expiratory volume in 1 s = 40 +/- 3%predicted; mean +/- SE) inhaled tiotropium 18 mug or placebo once daily for 7-10 days each. Pulmonary function tests and symptom-limited cycle exercise at 75% of each patient's maximal work capacity were performed 2 h after dosing. Dyspnea intensity (Borg scale), operating lung volumes, breathing pattern, and esophageal pressure (n = 11) were measured during exercise. Dynamic hyperinflation reached its maximal value early in exercise and was associated with only mild increases in dyspnea intensity and the effort-displacement ratio, which is defined as the ratio between tidal swings of esophageal pressure (expressed relative to maximum inspiratory pressure) and Vt (expressed relative to predicted vital capacity). After a minimal IRV of 0.5 +/- 0.1 liter was reached, both dyspnea and the effort-displacement ratio rose steeply until an intolerable level was reached. Tiotropium did not alter dyspnea-IRV relationships, but the increase in resting and exercise inspiratory capacity was associated with an improved effort-displacement ratio throughout exercise. Once a critically low IRV was reached during exercise, dyspnea rose with the disparity between respiratory effort and the Vt response. Changes in dyspnea intensity after tiotropium were positively correlated with changes in this index of neuromechanical coupling.
在慢性阻塞性肺疾病患者进行恒功运动时，一旦吸气储备量（IRV）降至阻止潮气量（Vt）进一步扩大的临界水平，呼吸困难会急剧增加。我们研究了这种机械限制对运动性呼吸困难的质量和强度的影响，并考察了一种抗胆碱能支气管扩张剂的作用。在一项随机、双盲、交叉研究中，18例慢性阻塞性肺疾病患者（第1秒用力呼气量=预测值的40±3%；均值±标准误）每天吸入18μg噻托溴铵或安慰剂，各持续7 - 10天。给药后2小时进行肺功能测试和以每位患者最大工作能力的75%进行症状限制性周期运动。运动期间测量呼吸困难强度（Borg量表）、工作肺容积、呼吸模式和食管压力（n = 11）。动态肺过度充气在运动早期达到最大值，且仅与呼吸困难强度和用力-位移比值的轻度增加相关，用力-位移比值定义为食管压力的潮气量波动（相对于最大吸气压力表示）与Vt（相对于预测肺活量表示）之比。在达到最小IRV为0.5±0.1升后，呼吸困难和用力-位移比值均急剧上升，直至达到无法耐受的水平。噻托溴铵未改变呼吸困难-IRV关系，但静息和运动吸气能力的增加与整个运动过程中用力-位移比值的改善相关。运动期间一旦达到极低的IRV，呼吸困难会随着呼吸用力与Vt反应之间的差异而增加。噻托溴铵治疗后呼吸困难强度的变化与这种神经机械耦联指标的变化呈正相关。
