Antiadrenergic effects of adenosine on His-Purkinje automaticity. Evidence for accentuated antagonism.
Antiadrenergic effects of adenosine on His-Purkinje automaticity. Evidence for accentuated antagonism.
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腺苷对希氏-浦肯野自动性的抗肾上腺素作用。
DOI：
10.1172/jci113834
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Belardinelli,L
中科院分区：
文献类型：
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作者：
Lerman,BB;WesleyJr,RC;DiMarco,JP;Haines,DE;Belardinelli,L
本文观察了腺苷对9例完全性房室传导阻滞患者希氏-浦肯野系统（HPS）的影响。腺苷对对照组HPS周期长度的影响最小，但在异丙肾上腺素的存在下，它从906 +/- 183增加到1，449 +/- 350 ms，P <0.001。竞争性腺苷拮抗剂氨茶碱可完全消除腺苷的这种抗肾上腺素能作用。在手术诱导房室传导阻滞的离体豚鼠心脏中，异丙肾上腺素使HPS率降低36%，而在1，3-二丙基-8-苯基-黄嘌呤（一种有效的腺苷拮抗剂）存在下，HPS率降低48%，并与腺苷释放增加相关。因此，通过在受体水平阻断腺苷的作用，腺苷拮抗儿茶酚胺作用的生理负反馈机制被解偶联。本研究的结果表明，腺苷对人类HPS的影响主要是抗肾上腺素能的，因此与增强拮抗作用的概念一致。腺苷的这些作用可能作为一种反调节代谢反应，改善了由增强的交感神经张力扰动的O2供需比。在局部缺血或肾上腺素能应激增强期间发生的一些儿茶酚胺介导的室性心律失常可能是由于这种负反馈系统的失衡。
The effects of adenosine on the human His-Purkinje system (HPS) were studied in nine patients with complete atrioventricular (AV) block. Adenosine had minimal effect on the control HPS cycle length, but in the presence of isoproterenol increased it from 906 +/- 183 to 1,449 +/- 350 ms, P less than 0.001. Aminophylline, a competitive adenosine antagonist, completely abolished this antiadrenergic effect of adenosine. In isolated guinea pig hearts with surgically induced AV block, isoproterenol decreased the HPS rate by 36%, whereas in the presence of 1,3-dipropyl-8-phenyl-xanthine, a potent adenosine antagonist, the HPS rate decreased by 48% and was associated with an increased release of adenosine. Therefore, by blocking the effects of adenosine at the receptor level, the physiologic negative feedback mechanism by which adenosine antagonizes the effects of catecholamines was uncoupled. The results of this study indicate that adenosine's effects on the human HPS are primarily antiadrenergic and are thus consistent with the concept of accentuated antagonism. These effects of adenosine may serve as a counterregulatory metabolic response that improves the O2 supply-demand ratio perturbed by enhanced sympathetic tone. Some catecholamine-mediated ventricular arrhythmias that occur during ischemia or enhanced adrenergic stress may be due to an imbalance in this negative feedback system.