Lai W T, Lee C S, Wu J C, Sheu S H, Wu S N
Department of Internal Medicine, Kaohsiung Medical College, Taiwan, Republic of China.
Am Heart J. 1996 Oct;132(4):768-75. doi: 10.1016/s0002-8703(96)90309-9.
Adenosine, verapamil, propranolol, and procainamide are widely used antiarrhythmic drugs. The interactions among them are still not known in human beings. Adenosine-induced negative dromotropic effects were assessed by rapid bolus injection of adenosine during constant high right atrial pacing in each patient. The initial dose of adenosine was 0.5 mg and was followed by a stepwise increment of 0.5 mg until atrioventricular (AV) nodal block occurred. The negative dromotropic actions of adenosine were examined in the control state and in the following three protocols in three groups of patients: (1) In 12 patients (group 1), intravenous verapamil, 0.15 mg/kg, was given; (2) In 12 patients (group 2), intravenous propranolol, 0.1 mg/kg, was given; and (3) in 10 patients (group 3), intravenous procainamide, 15 mg/kg, was given. The dose-response curves of adenosine on AV nodal conduction were almost identical in the control state and after verapamil, propranolol, or procainamide injection. However, verapamil, in contrast to propranolol, significantly reduced the dose of adenosine required to produce AV nodal block, from 4.4 +/- 0.7 mg to 2.7 +/- 0.3 mg (p < 0.01). Of note, procainamide exerted no significant effects on adenosine-induced negative dromotropism on AV nodal conduction or AV nodal block. In conclusion, the negative dromotropic effects of adenosine are preserved and independent even in the presence of verapamil, propranolol, or procainamide. Both verapamil and propranolol can exhibit additive effects with adenosine in prolonging AV nodal conduction time; however, only verapamil can reduce the dose of adenosine required to produce AV nodal block. This finding indicates that the dose of adenosine may be reduced for patients who have already been treated with verapamil.
腺苷、维拉帕米、普萘洛尔和普鲁卡因胺是广泛使用的抗心律失常药物。它们之间的相互作用在人体中仍不明确。在每位患者持续高频率右心房起搏期间，通过快速推注腺苷来评估腺苷诱导的负性变传导作用。腺苷的初始剂量为0.5毫克，随后每次递增0.5毫克，直至发生房室（AV）结阻滞。在三组患者中，分别在对照状态以及以下三种方案下检查腺苷的负性变传导作用：（1）12例患者（第1组）静脉注射维拉帕米，剂量为0.15毫克/千克；（2）12例患者（第2组）静脉注射普萘洛尔，剂量为0.1毫克/千克；（3）10例患者（第3组）静脉注射普鲁卡因胺，剂量为15毫克/千克。在对照状态以及注射维拉帕米、普萘洛尔或普鲁卡因胺后，腺苷对房室结传导的剂量 - 反应曲线几乎相同。然而，与普萘洛尔相比，维拉帕米显著降低了产生房室结阻滞所需的腺苷剂量，从4.4±0.7毫克降至2.7±0.3毫克（p<0.01）。值得注意的是，普鲁卡因胺对腺苷诱导的房室结传导负性变传导作用或房室结阻滞无显著影响。总之，即使存在维拉帕米、普萘洛尔或普鲁卡因胺，腺苷的负性变传导作用仍然存在且相互独立。维拉帕米和普萘洛尔在延长房室结传导时间方面均可与腺苷表现出相加作用；然而，只有维拉帕米能降低产生房室结阻滞所需的腺苷剂量。这一发现表明，对于已经接受维拉帕米治疗的患者，可能需要减少腺苷的剂量。
