Malcolm A D, Garratt C J, Camm A J
Department of Cardiological Sciences, St. George's Hospital Medical School, London, England.
Cardiovasc Drugs Ther. 1993 Feb;7(1):139-47. doi: 10.1007/BF00878323.
Adenosine is a purine nucleoside with a rapid onset and brief duration of action after intravenous bolus administration. Its most prominent cardiac effect is impairment or blockade of atrioventricular nodal conduction, but other effects are depression of automaticity of the sinus node and attenuation of catecholamine-related ventricular after-depolarizations. The cardiac cell surface receptor is the A1 purinoceptor. The therapeutic value of adenosine is predominantly in those arrhythmias in which the atrioventricular node forms part of a reentry circuit, as clearly demonstrated by the high success rate for termination of atrioventricular nodal reentry tachycardia and of atrioventricular reentry tachycardia involving an accessory pathway in the Wolff-Parkinson-White syndrome. Ventricular tachycardias are generally unresponsive, with the exception of right ventricular outflow tract tachycardia. A diagnostic role has emerged for adenosine. The transient blockade of the atrioventricular node that it causes can reveal important electrocardiographic features in arrhythmias, such as atrial flutter, or can unmask latent preexcitation. In wide-QRS tachycardias, adenosine can help to distinguish ventricular tachycardia from supraventricular tachycardia with QRS aberration. Unlike verapamil, adenosine is safe in ventricular tachycardia. A suggested dosing scheme is to give incremental doses at 1-minute intervals, starting at 0.05 mg/kg and continuing until complete atrioventricular block is induced or a maximum of 0.25 mg/kg is reached. Side effects are transient, sometimes uncomfortable, and not hazardous; dyspnea and chest discomfort are most frequent. A history of asthma is a relative contraindication. Aminophylline antagonizes and dipyridamole potentiates the effects of adenosine.
腺苷是一种嘌呤核苷，静脉推注给药后起效迅速，作用持续时间短暂。其最显著的心脏效应是损害或阻断房室结传导，但其他效应包括抑制窦房结自律性以及减轻儿茶酚胺相关的心室后除极。心脏细胞表面受体为A1嘌呤受体。腺苷的治疗价值主要体现在那些房室结构成折返环一部分的心律失常中，这在终止房室结折返性心动过速以及预激综合征中涉及旁路的房室折返性心动过速时的高成功率中得到了明确体现。室性心动过速一般对腺苷无反应，但右心室流出道心动过速除外。腺苷已显示出诊断作用。它所引起的房室结短暂阻断可揭示心律失常中的重要心电图特征，如心房扑动，或可暴露潜在的预激。在宽QRS波心动过速中，腺苷有助于将室性心动过速与伴有QRS波畸变的室上性心动过速区分开来。与维拉帕米不同，腺苷在室性心动过速中是安全的。建议的给药方案是每隔1分钟递增给药，起始剂量为0.05mg/kg，持续给药直至诱发完全性房室传导阻滞或达到最大剂量0.25mg/kg。副作用是短暂的，有时会让人不适，但并无危害；呼吸困难和胸部不适最为常见。哮喘病史是相对禁忌证。氨茶碱可拮抗腺苷的作用，双嘧达莫则可增强腺苷的作用。
