Iijima T, Taira N
Eur J Pharmacol. 1976 May;37(1):55-62. doi: 10.1016/0014-2999(76)90007-8.
In isolated and cross-circulated canine A-V node preparations single injections of Mn2+ (1-30 mumol) and verapamil (0.3-10 nmol) into the posterior septal artery (PSA) caused a dose-dependent increase in the A-V conduction time and, in large doses, produced A-V conduction block. The A-V conduction time increased by Mn2+ and verapamil is resotred by 1-norepinephrine (1-NE) injected into the PSA. The A-V nodal tachycardia induced by 1-NE is suppressed by Mn2+ but not by verapamil. These indicate the following: (1) the slow Ca2+ channel plays an important role in A-V conduction; (2) the positive dromotropic response of the A-V node to 1-NE may have some relations to the Ca2+ channel; (3) the A-V nodal tachycardia induced by 1-NE may be mediated by the Ca2+ channel. Possible causes which produced differences between Mn2+ and verapamil in the effects in antagonizing the 1-NE-induced A-V nodal tachycardia are discussed.
在分离并交叉循环的犬房室结标本中，向后间隔动脉（PSA）单次注射锰离子（1 - 30微摩尔）和维拉帕米（0.3 - 10纳摩尔）会导致房室传导时间呈剂量依赖性增加，大剂量时会产生房室传导阻滞。由锰离子和维拉帕米导致增加的房室传导时间可通过向PSA注射1 - 去甲肾上腺素（1 - NE）得以恢复。由1 - NE诱发的房室结性心动过速可被锰离子抑制，但不能被维拉帕米抑制。这些表明：（1）慢钙通道在房室传导中起重要作用；（2）房室结对1 - NE的正向变传导反应可能与钙通道有某些关系；（3）由1 - NE诱发的房室结性心动过速可能由钙通道介导。文中讨论了在拮抗1 - NE诱发的房室结性心动过速的作用中，锰离子和维拉帕米产生差异的可能原因。
