Effects of Aerosolized Adenosine 5′-Triphosphate in Smokers and Patients With COPD
＜背景＞
細胞外のアデノシン5' ３リン酸（ＡＴＰ）は肺の迷走神経ＣおよびＡδ線維を刺激し，
迷走神経終末に位置するＰ２Ｘ２／３受容体を介して気管支収縮，咳を誘発する．
我々は正常人，健康喫煙者，ＣＯＰＤ患者においてＡＴＰのネブライザーが咳や症状に与える影響を調べ，
ＡＴＰの代謝産物であるアデノシンを吸入した場合と比較した．
＜方法＞
非喫煙者１０名，喫煙者１４名，ＣＯＰＤ患者７名において，ＡＴＰおよびアデノシン１リン酸（ＡＭＰ）のネブライザー吸入を行い，
気道径，Borgスコアで表した呼吸困難，咳の感受性，呼気中のＡＴＰ濃度を調べた．
＜結果＞
正常人と比較して喫煙者，ＣＯＰＤ患者ではＡＴＰはより呼吸困難，咳，のどのイガイガ感を誘発した．
ＡＴＰはＡＭＰよりも差がはっきり出た．
ＣＯＰＤ患者の呼気中のＡＴＰ濃度は正常人よりも増加していた．
＜感想＞
ＣＯＰＤ患者や喫煙者は細胞外のＡＴＰに対して正常人よりも過敏性が強いようです．
これがＣＯＰＤの病態に関連している可能性を筆者らは考察しています．
BACKGROUND: Extracellular adenosine 5′-triphosphate (ATP) stimulates vagal C and Aδ fibers in the lung, resulting in pronounced bronchoconstriction and cough mediated by P2X2/3 receptors located on vagal sensory nerve terminals. We investigated the effects of nebulized ATP on cough and symptoms in control subjects, healthy smokers, and patients with COPD and compared these responses to the effects of inhaled adenosine, the metabolite of ATP.
METHODS: We studied the effects of inhaled ATP and adenosine monophosphate (AMP) on airway caliber, perception of dyspnea assessed by the Borg score, cough sensitivity, and ATP in exhaled breath condensate in healthy nonsmokers (n = 10), healthy smokers (n = 14), and patients with COPD (n = 7).
RESULTS: In comparison with healthy subjects, ATP induced more dyspnea, cough, and throat irritation in smokers and patients with COPD, and the effects of ATP were more pronounced than those of AMP. The concentration of ATP in the exhaled breath condensate of patients with COPD was elevated compared with that of healthy subjects.
CONCLUSIONS: Smokers and patients with COPD manifest hypersensitivity to extracellular ATP, which may play a mechanistic role in COPD