Passannante A N, Hazucha M J, Bromberg P A, Seal E, Folinsbee L, Koch G
Department of Anesthesiology, School of Medicine, University of North Carolina at Chapel Hill, USA.
J Appl Physiol (1985). 1998 Nov;85(5):1863-70. doi: 10.1152/jappl.1998.85.5.1863.
We have previously suggested that ozone (O3)-induced pain-related symptoms and inhibition of maximal inspiration are due to stimulation of airway C fibers (M. J. Hazucha, D. V. Bates, and P. A. Bromberg. J. Appl. Physiol. 67: 1535-1541, 1989). If this were so, pain suppression or inhibition by opioid-receptor agonists should partially or fully reverse O3-induced symptomatic and lung functional responses. The objectives of this study were to determine whether O3-induced pain limits maximal inspiration and whether endogenous opioids contribute to modulation of the effects of inhaled O3 on lung function. The participants in this double-blind crossover study were healthy volunteers (18-59 yr) known to be "weak" (WR; n = 20) and "strong" O3 responders (SR; n = 42). They underwent either two 2-h exposures to air or two 2-h exposures to 0. 42 parts/million O3 with moderate intermittent exercise. Immediately after post-O3 spirometry, the WR were randomly given either naloxone (0.15 mg/kg iv) or saline, whereas SR randomly received either sufentanil (0.2 microgram/kg iv) or saline. O3 exposure significantly (P < 0.001) impaired lung function. In SR, sufentanil rapidly, although not completely, reversed both the chest pain and spirometric effects (forced expiratory volume in 1 s; P < 0.0001) compared with saline. Immediate postexposure administration of saline or naloxone had no significant effect on WR. Plasma beta-endorphin levels were not related to an individual's O3 responsiveness. Cutaneous pain variables showed a nonsignificant weak association with O3 responsiveness. These observations demonstrate that nociceptive mechanisms play a key role in modulating O3-induced inhibition of inspiration but not in causing lack of spirometric response to O3 exposure in WR.
我们之前曾提出，臭氧（O₃）诱发的疼痛相关症状以及对最大吸气的抑制是由于气道C纤维受到刺激（M. J. 哈祖查、D. V. 贝茨和P. A. 布罗姆伯格。《应用生理学杂志》67: 1535 - 1541, 1989）。如果真是这样，阿片受体激动剂对疼痛的抑制或抑制作用应该会部分或完全逆转O₃诱发的症状和肺功能反应。本研究的目的是确定O₃诱发的疼痛是否会限制最大吸气，以及内源性阿片类物质是否有助于调节吸入O₃对肺功能的影响。这项双盲交叉研究的参与者是健康志愿者（18 - 59岁），分为“弱”反应者（WR；n = 20）和“强”O₃反应者（SR；n = 42）。他们接受了两次2小时的空气暴露或两次2小时的0.42 ppm O₃暴露，并伴有适度的间歇运动。在O₃暴露后的肺活量测定后，WR被随机给予纳洛酮（0.15 mg/kg静脉注射）或生理盐水，而SR则随机接受舒芬太尼（0.2 μg/kg静脉注射）或生理盐水。O₃暴露显著（P < 0.001）损害了肺功能。在SR中，与生理盐水相比，舒芬太尼迅速（尽管不完全）逆转了胸痛和肺活量测定效应（1秒用力呼气量；P < 0.0001）。暴露后立即给予生理盐水或纳洛酮对WR没有显著影响。血浆β - 内啡肽水平与个体的O₃反应性无关。皮肤疼痛变量与O₃反应性呈非显著的弱关联。这些观察结果表明，伤害性感受机制在调节O₃诱发的吸气抑制中起关键作用，但在导致WR对O₃暴露缺乏肺活量测定反应方面不起作用。
