Takeda M, Furukawa Y, Ogiwara Y, Saegusa K, Haniuda M, Akahane K, Chiba S
Department of Pharmacology, Shinshu University School of Medicine, Matsumoto, Japan.
Arch Int Pharmacodyn Ther. 1989 Jan-Feb;297:39-48.
The effects of the bradycardic agents alinidine and falipamil, on atrio-ventricular (AV) conduction were compared with those of other negative chronotropic agents, acetylcholine (ACh), carbachol (CCh), adenosine and verapamil, in open-chest, anesthetized dogs. When each drug was selectively administered into the AV node artery, none of them changed the sinus rate and arterial blood pressure. Although alinidine did not significantly change the atrio-ventricular conduction time (AVCT), falipamil and others induced a dose-dependent prolongation of the AVCT. The order of the AVCT prolongation was CCh greater than ACh greater than verapamil much greater than adenosine greater than falipamil much greater than alinidine. ACh, CCh and verapamil frequently caused second or third degree AV block at higher doses. The His bundle electrocardiogram revealed that all AV blocks occurred between the atrium and the His bundle (A-H block). The CCh-induced prolongation of the AVCT, but not the adenosine-induced prolongation, was significantly suppressed by treatment with alinidine or falipamil. These results indicate that alinidine scarcely affects AV conduction in the in situ dog heart and that the muscarinic cholinergic receptor blocking effect of alinidine or falipamil modifies the AVCT secondarily when vagal activity is maintained.
在开胸麻醉犬中，将心动过缓药物阿利尼定和法利帕米对房室（AV）传导的影响与其他负性变时性药物乙酰胆碱（ACh）、卡巴胆碱（CCh）、腺苷和维拉帕米进行了比较。当每种药物选择性地注入房室结动脉时，它们均未改变窦性心律和动脉血压。虽然阿利尼定未显著改变房室传导时间（AVCT），但法利帕米和其他药物可引起AVCT剂量依赖性延长。AVCT延长的顺序为CCh＞ACh＞维拉帕米＞＞腺苷＞＞法利帕米＞＞阿利尼定。ACh、CCh和维拉帕米在较高剂量时经常引起二度或三度房室传导阻滞。希氏束心电图显示，所有房室传导阻滞均发生在心房和希氏束之间（A-H阻滞）。阿利尼定或法利帕米治疗可显著抑制CCh诱导的AVCT延长，但不能抑制腺苷诱导的延长。这些结果表明，阿利尼定对犬原位心脏的房室传导几乎没有影响，并且当迷走神经活性保持时，阿利尼定或法利帕米的毒蕈碱胆碱能受体阻断作用会继发改变AVCT。
