Misuri G, Mancini M, Iandelli I, Duranti R, Stendardi L, Gigliotti F, Rosi E, Ronchi M C, Scano G
Section of Respiratory Rehabilitation, Fondazione Pro-Juventute Don Carlo Gnocchi, Pozzolatico, Florence, Italy.
Pulm Pharmacol Ther. 1997 Oct-Dec;10(5-6):299-304. doi: 10.1006/pupt.1998.0108.
Whether, and to what extent, beta 2-agonists protect against respiratory muscle overloading and breathlessness during bronchoconstriction remains to be defined in patients with asthma. In a double blind placebo-controlled study, 100 micrograms of fenoterol were administered to six stable asthmatics before a bronchial provocation test, performed by inhaling doubling concentrations of histamine from a Devilbiss 646 nebulizer. We recorded breathing pattern (tidal volume VT, inspiratory time TI, total time of the respiratory cycle TTOT), inspiratory capacity (IC), dynamic pleural pressure swing (Pplsw), total lung resistance (RL) and FEV1. VT was expressed both in actual values and as % of IC. Changes in VT (%IC) during histamine inhalation reflected changes in dynamic end-inspiratory lung volume (EILV). Pplsw was expressed as % of maximal (the most negative in sign) pleural pressure, obtained under control conditions during a sniff manoeuvre (Pplsn). Pplsw (%Pplsn) is an index of inspiratory muscle effort. The test ended when the concentration of histamine which caused a decrease in FEV1 of > or = 40% post-saline was reached. Dyspnoea rating was scored by a modified Borg scale. At the ultimate degree of bronchoconstriction (UDB) with histamine: (i) decrease in FEV1 was similar after placebo and fenoterol, while increase in RL was lower after fenoterol (P < 0.005); (ii) VT(%IC) increased less after fenoterol (P < 0.027); (iii) increases in Pplsw (%Pplsn) was lower after fenoterol (P < 0.001); (iv) delta Borg (from saline) was lower (P < 0.01) after fenoterol; (v) differences in delta Borg, from placebo to fenoterol, related to concurrent changes in VT(%IC) (r2 = 0.67). In conclusion, at UDB 100 micrograms of fenoterol produced a beneficial effect on the degree of inspiratory muscle loading and breathlessness, an effect greater than it would be expected from measuring FEV1 alone.
在哮喘患者中，β2 激动剂是否以及在何种程度上能预防支气管收缩期间呼吸肌负荷过重和呼吸困难仍有待确定。在一项双盲安慰剂对照研究中，对 6 名病情稳定的哮喘患者在支气管激发试验前给予 100 微克非诺特罗，该试验通过使用德维比斯 646 雾化器吸入成倍浓度的组胺来进行。我们记录了呼吸模式（潮气量 VT、吸气时间 TI、呼吸周期总时间 TTOT）、吸气容量（IC）、动态胸膜压力波动（Pplsw）、总肺阻力（RL）和第一秒用力呼气容积（FEV1）。VT 以实际值和占 IC 的百分比表示。组胺吸入期间 VT（%IC）的变化反映了动态吸气末肺容积（EILV）的变化。Pplsw 以在嗅吸动作（Pplsn）的对照条件下获得的最大（最负）胸膜压力的百分比表示。Pplsw（%Pplsn）是吸气肌努力程度的指标。当达到使盐水激发后 FEV1 降低≥40%的组胺浓度时，试验结束。呼吸困难程度采用改良的博格量表评分。在组胺导致的最大支气管收缩程度（UDB）时：（i）安慰剂和非诺特罗后 FEV1 的降低相似，而非诺特罗后 RL 的增加较低（P<0.005）；（ii）非诺特罗后 VT（%IC）增加较少（P<0.027）；（iii）非诺特罗后 Pplsw（%Pplsn）的增加较低（P<0.001）；（iv）非诺特罗后δ博格（相对于盐水激发）较低（P<0.01）；（v）从安慰剂到非诺特罗的δ博格差异与 VT（%IC）的同时变化相关（r2 = 0.67）。总之，在 UDB 时，100 微克非诺特罗对吸气肌负荷程度和呼吸困难产生有益影响，该影响大于仅通过测量 FEV1 所预期的效果。
