Differential effects of airway anesthesia on ozone-induced pulmonary responses in human subjects.

Differential effects of airway anesthesia on ozone-induced pulmonary responses in human subjects.
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气道麻醉对人类受试者臭氧引起的肺部反应的不同影响。

DOI:
10.1164/ajrccm.163.5.2003103
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发表时间:
2001
期刊:
American journal of respiratory and critical care medicine.
影响因子:
--
通讯作者:
Adams,WC
Adams,WC
中科院分区:
--
文献类型:
--
作者:
Schelegle,ES;Eldridge,MW;Cross,CE;Walby,WF;Adams,WC

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我们观察了局部麻醉剂丁卡因雾化吸入对22名臭氧敏感健康受试者急性吸入0.30ppm臭氧65min引起的肺容量减少、快速浅呼吸和呼吸不适的主观症状的影响。臭氧吸入50min后,FEV1降低24%,呼吸频率增加40%,潮气量减少31%,总主观症状评分增加(71.2分,过滤空气暴露3.8分)。吸入丁卡因气雾剂后,臭氧引起的咽喉发痒和/或刺激(92.1%)、咳嗽(78.5%)、呼吸急促(72.5%)和深吸入性疼痛(69.4%)等主观症状明显减少。相比之下,吸入丁卡因气雾剂(空气动力学质量中值直径为3.52μm,几何标准差为1.92)仅导致轻微且不一致的FEV1下降(5.0%)和呼吸频率(−3.8%),与生理盐水气雾剂(FEV1 5.1%和呼吸频率−2.7%)无显著差异。我们的数据与位于气管-支气管树大型传导气道内的传入终末是主要负责臭氧诱导的主观症状是一致的,并提供了强有力的证据,表明臭氧诱导的对最大吸气努力的抑制不依赖于吸气不适的有意识感觉。
We examined the effect of tetracaine aerosol inhalation, a local anesthetic, on lung volume decrements, rapid shallow breathing, and subjective symptoms of breathing discomfort induced by the acute inhalation of 0.30 ppm ozone for 65 min in 22 ozone-sensitive healthy human subjects. After 50 min of ozone inhalation FEV1was reduced 24%, breathing frequency was increased 40%, tidal volume was decreased 31%, and total subjective symptom score was increased (71.2, compared with 3.8 for filtered air exposure). Inhalation of tetracaine aerosol resulted in marked reductions in ozone-induced subjective symptoms of throat tickle and/or irritation (92.1%), cough (78.5%), shortness of breath (72.5%), and pain on deep inspiration (69.4%). In contrast, inhalation of tetracaine aerosol (mass median aerodynamic diameter of 3.52 μ m with a geometric standard deviation of 1.92) resulted in only minor and inconsistent rectification of FEV1decrements (5.0%) and breathing frequency ( − 3.8%) that was not significantly different from that produced by saline aerosol alone (FEV1, 5.1% and breathing frequency, − 2.7%). Our data are consistent with afferent endings located within the large conducting airways of the tracheobronchial tree being primarily responsible for ozone-induced subjective symptoms and provides strong evidence that ozone-induced inhibition of maximal inspiratory effort is not dependent on conscious sensations of inspiratory discomfort.