Pauwels R A, Van der Straeten M E
Am Rev Respir Dis. 1987 Aug;136(2):374-8. doi: 10.1164/ajrccm/136.2.374.
The inhalation of adenosine is known to cause bronchoconstriction in asthmatic patients. A thorough study of the possible role of this purine nucleoside in the pathogenesis of asthma has been hampered by the lack of a suitable animal model. We have studied the bronchial effects of adenosine in an in vivo rat model. The intravenous injection of 0.1 to 10 micromoles/kg body weight of adenosine causes in BDE-rats an increase in lung resistance and decrease in dynamic compliance. Study of the potency of various adenosine analogs suggests that the bronchial adenosine receptor belongs to the A2-type. The bronchoconstriction caused by adenosine is inhibited by atropine, methysergide, sodium cromoglycate, nedocromil sodium, and ketotifen. Xanthines in doses of 5 and 15 mg/kg body weight have no significant effect on the adenosine-induced bronchoconstriction. These results suggest that adenosine causes bronchoconstriction by stimulating postsynaptic vagal nerve endings and mast cells.
已知吸入腺苷会导致哮喘患者支气管收缩。由于缺乏合适的动物模型,对这种嘌呤核苷在哮喘发病机制中可能作用的深入研究受到了阻碍。我们在大鼠体内模型中研究了腺苷对支气管的影响。静脉注射0.1至10微摩尔/千克体重的腺苷会使BDE大鼠的肺阻力增加,动态顺应性降低。对各种腺苷类似物效力的研究表明,支气管腺苷受体属于A2型。腺苷引起的支气管收缩可被阿托品、甲基麦角新碱、色甘酸钠、奈多罗米钠和酮替芬抑制。体重5毫克/千克和15毫克/千克剂量的黄嘌呤对腺苷诱导的支气管收缩无显著影响。这些结果表明,腺苷通过刺激突触后迷走神经末梢和肥大细胞引起支气管收缩。