Popa V
Clin Pharmacol Ther. 1986 Sep;40(3):329-37. doi: 10.1038/clpt.1986.184.
In nine patients with asthma and 11 normal subjects, by means of specific airway conductance (Gaw/VL) and flow volume loops, we measured: resting airway caliber, bronchodilation after 0.75 and 1.50 mg of quantitatively inhaled atropine (A0.75 and A1.50), provocation dose-40 of acetylcholine (ACH) (PD40-ACH), dose ratio of ACH (DR-ACH) after saline solution, A0.75 and A1.50, and the slope of log-dose response curves to ACH (SLDRC-ACH). Normal and asthmatic subjects showed different PD40-ACH (1.26 +/- 1.37 mg and 0.34 +/- 0.32 mg) but similar resting Gaw/VL, delta Gaw/VL after A0.75 or A1.50, DR-ACH after A0.75, and SLDRC-ACH. There was no correlation between atropine-induced bronchodilatation PD40-ACH or any of the above-mentioned tests. We conclude that in normal subjects and in those with asthma, extramuscarinic or postmuscarinic receptor mechanisms may account for the presence of comparable atropine-induced bronchodilatation and resting Gaw/VL in spite of widely different PD40-ACH. The regulatory site responsible for PD40-ACH, the only test separating asthmatics from normal subjects, seemingly is located downstream from the regulatory site of other nondiscriminative tests.
在9例哮喘患者和11名正常受试者中,我们通过比气道传导率(Gaw/VL)和流量-容积环测量了:静息气道管径、定量吸入0.75 mg和1.50 mg阿托品(A0.75和A1.50)后的支气管舒张、乙酰甲胆碱(ACH)激发剂量-40(PD40-ACH)、生理盐水、A0.75和A1.50后ACH的剂量比(DR-ACH)以及ACH对数剂量反应曲线的斜率(SLDRC-ACH)。正常受试者和哮喘患者的PD40-ACH不同(分别为1.26±1.37 mg和0.34±0.32 mg),但静息Gaw/VL、A0.75或A1.50后的Gaw/VL变化、A0.75后的DR-ACH以及SLDRC-ACH相似。阿托品诱导的支气管舒张、PD40-ACH与上述任何一项测试之间均无相关性。我们得出结论,在正常受试者和哮喘患者中,尽管PD40-ACH差异很大,但毒蕈碱外或毒蕈碱后受体机制可能是阿托品诱导的支气管舒张和静息Gaw/VL相当的原因。负责PD40-ACH的调节位点,是唯一能区分哮喘患者与正常受试者的测试,似乎位于其他无鉴别性测试的调节位点的下游。