Crimi N, Polosa R, Mistretta A
Recenti Prog Med. 1989 Jul-Aug;80(7-8):372-6.
Adenosine has been found to contract human bronchial smooth muscle in vitro and to induce bronchoconstriction in asthmatic patients when administered by inhalation. The importance of adenosine for bronchial tone and bronchial reactivity is still unclear. Adenosine seems unlikely to cause bronchoconstriction by a non-specific irritant effect. Some evidence suggests that the action of adenosine relates to a specific pharmacologic activity. Bronchoconstriction induced by adenosine is antagonized by theophylline and is potentiated by dipyridamole. Therapeutic concentrations of theophylline exhibit specificity for adenosine's bronchoconstrictor activity supporting the concept that the bronchospastic effect of adenosine is mediated through stimulation of cell surface receptors. Stimulation of afferent receptors producing vagally mediated reflex seems unlikely. A further explanation of adenosine bronchoconstriction is a release of mediators through potentiation of ongoing mediator release from bronchial luminal mast-cells.
已发现腺苷在体外可使人类支气管平滑肌收缩，且通过吸入给药时可诱发哮喘患者的支气管收缩。腺苷对支气管张力和支气管反应性的重要性仍不清楚。腺苷似乎不太可能通过非特异性刺激作用引起支气管收缩。一些证据表明，腺苷的作用与特定的药理活性有关。腺苷诱导的支气管收缩可被茶碱拮抗，而双嘧达莫可使其增强。治疗浓度的茶碱对腺苷的支气管收缩活性具有特异性，这支持了腺苷的支气管痉挛效应是通过刺激细胞表面受体介导的这一概念。通过刺激传入受体产生迷走神经介导的反射似乎不太可能。腺苷支气管收缩的另一种解释是通过增强支气管腔内肥大细胞持续释放介质来释放介质。
