Morrison J F, Pearson S B, Dean H G
Pulmonary Function Laboratory, Killingbeck Hospital, Leeds.
Br Med J (Clin Res Ed). 1988 May 21;296(6634):1427-9. doi: 10.1136/bmj.296.6634.1427.
To investigate the effect of vagal blockade with atropine on nocturnal fall in peak expiratory flow rate 10 patients with asthma who had a diurnal variation in peak expiratory flow rate of greater than 20% were given 30 micrograms/kg of intravenous atropine or a placebo at 4 am and 4 pm. Vagal blockade caused significant bronchodilatation at 4 am and 4 pm (peak expiratory flow rate rose from 260 to 390 l/min at 4 am and 400 to 440 l/min at 4 pm) and significantly increased the pulse rate from 60 to 121 beats/minute at 4 am and from 76 to 122 beats/minute at 4 pm. Nocturnal asthma was almost totally reversed, implying that vagal mechanisms are fundamental in its pathophysiology. Other mechanisms--diurnal changes in plasma adrenaline concentration, the activity of non-adrenergic non-cholinergic nerves, and circadian rhythms of inflammatory mediator activity--may also be implicated.
为研究阿托品迷走神经阻滞对夜间呼气峰值流速下降的影响,对10名哮喘患者进行了研究,这些患者呼气峰值流速的日变化率大于20%,于凌晨4点和下午4点给予他们30微克/千克静脉注射阿托品或安慰剂。迷走神经阻滞在凌晨4点和下午4点引起了显著的支气管扩张(凌晨4点呼气峰值流速从260升/分钟升至390升/分钟,下午4点从400升/分钟升至440升/分钟),并使脉搏率显著增加,凌晨4点从60次/分钟升至121次/分钟,下午4点从76次/分钟升至122次/分钟。夜间哮喘几乎完全得到逆转,这意味着迷走神经机制在其病理生理学中起着根本作用。其他机制——血浆肾上腺素浓度的日变化、非肾上腺素能非胆碱能神经的活性以及炎症介质活性的昼夜节律——也可能与之相关。