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吸入纳洛酮对静息支气管张力和运动诱发性哮喘的影响。

The effect of inhaled naloxone on resting bronchial tone and exercise-induced asthma.

作者信息

Popa V, Rients P

机构信息

Department of Medicine, University of California, Davis, Sacramento 95823.

出版信息

Am Rev Respir Dis. 1989 Mar;139(3):702-9. doi: 10.1164/ajrccm/139.3.702.

DOI:10.1164/ajrccm/139.3.702
PMID:2923371
Abstract

UNLABELLED

We wanted to determine whether 10 mg naloxone inhaled quantitatively could modulate the resting bronchial tone and respiratory response in exercise-induced asthma (EIA). In 11 asthmatic subjects, we measured specific airway conductance (SGaw) and forced expiratory flow (FEF) before and after the inhalation of naloxone or saline. In another 10 asthmatic subjects, we measured SGaw, FEF, and the ventilatory gas exchange, heart rate, and blood pressure responses produced by a treadmill exercise during 3 separate days: without any pretreatment (Day 1) or preceded by the inhalation of either 10 mg naloxone (Day 2) or saline (Day 3). We found that after 10 mg inhaled naloxone only one of 11 subjects bronchodilated, displaying an isolated, reproducible delta SGaw greater than 40% at 30 and 60 min. In the EIA protocol, the cardiopulmonary responses during exercise remained similar on all experimental days, but in seven of 10 subjects (all with %FEV1/FVC greater than or equal to 70% delta SGaw was -60 +/- 11%, + 1 +/- 40%, and -52 +/- 7% during no treatment, naloxone, and saline days, respectively (p less than 0.05). FEF changes were comparable on all days (p greater than 0.05).

IN CONCLUSION

(1) consistent with the general role of endogenous opioids, these neurotransmitter/neuromodulators can modulate a stress-related bronchoconstrictor response (EIA), but only very seldom the resting bronchial tone. (2) Naloxone does not blunt EIA through a decrease in the asthmogenic stimulus (i.e., ventilation) or airway caliber change, but presumably through competition with the endogenous opioids released during exercise.

摘要

未标记

我们想确定定量吸入10毫克纳洛酮是否能调节运动诱发性哮喘(EIA)患者的静息支气管张力和呼吸反应。在11名哮喘患者中,我们测量了吸入纳洛酮或生理盐水前后的比气道传导率(SGaw)和用力呼气流量(FEF)。在另外10名哮喘患者中,我们在3个不同的日子里测量了SGaw、FEF以及跑步机运动引起的通气气体交换、心率和血压反应:无任何预处理(第1天),或在吸入10毫克纳洛酮(第2天)或生理盐水(第3天)之后。我们发现,吸入10毫克纳洛酮后,11名受试者中只有1人出现支气管扩张,在30分钟和60分钟时显示出孤立的、可重复的SGaw变化大于40%。在EIA方案中,所有实验日运动期间的心肺反应相似,但在10名受试者中的7人(所有FEV1/FVC%大于或等于70%)中,未治疗日、纳洛酮日和生理盐水日期间的SGaw变化分别为-60±11%、+1±40%和-52±7%(p<0.05)。所有日子里FEF变化具有可比性(p>0.05)。

结论

(1)与内源性阿片类物质的一般作用一致,这些神经递质/神经调节剂可调节与应激相关的支气管收缩反应(EIA),但很少调节静息支气管张力。(2)纳洛酮并非通过减少致喘刺激(即通气)或气道口径变化来减轻EIA,而是可能通过与运动期间释放的内源性阿片类物质竞争来实现。

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