Sugiyama S, Ozawa T, Suzuki S, Kato T
J Electrocardiol. 1980;13(1):49-54. doi: 10.1016/s0022-0736(80)80009-4.
This study was designed to determine whether or not verapamil and propranolol affect the lowering of the ventricular multiple response threshold (VMRT) that is seen following release of a previously ligated coronary artery. In mongrel dogs, the left anterior descending coronary artery was occluded for 15 min and then the ligation was released. The dogs were divided into three groups: in the control group, saline was administrated immediately before the release of ligation; in the two other groups, verapamil or propranolol were administrated immediately before the release of ligation. In the control group, VMRT was decreased during coronary occlusion and did not recover immediately after coronary recirculation. That is, significantly lowered values were observed at 5 and 10 min after reperfusion. The administration of verapamil prevented the lowering of VMRT after reperfusion, whereas propranolol had no effect. In all three groups, an increase in the difference of the concentration of K+ between the great cardiac vein and the femoral vein (delta K+) was observed soon after occlusion; however, delta K+ returned to normal soon after reperfusion. These results and the known anti-arrhythmic mechanism of verapamil suggests that Ca++-dependent action potentials might play an important role in lowering VMRT after release of a previously occluded coronary artery, whereas the effects of K+ and catecholamine do not play a role in causing the lowering of VMRT.
本研究旨在确定维拉帕米和普萘洛尔是否会影响在先前结扎的冠状动脉松解后出现的心室多重反应阈值(VMRT)降低。在杂种犬中,左前降支冠状动脉闭塞15分钟,然后松开结扎。犬被分为三组:对照组在松开结扎前立即给予生理盐水;另外两组在松开结扎前立即给予维拉帕米或普萘洛尔。对照组中,VMRT在冠状动脉闭塞期间降低,冠状动脉再灌注后未立即恢复。也就是说,在再灌注后5分钟和10分钟观察到显著降低的值。维拉帕米的给药可防止再灌注后VMRT降低,而普萘洛尔则无作用。在所有三组中,闭塞后不久观察到心大静脉和股静脉之间K+浓度差(ΔK+)增加;然而,再灌注后不久ΔK+恢复正常。这些结果以及维拉帕米已知的抗心律失常机制表明,钙依赖性动作电位可能在先前闭塞的冠状动脉松解后VMRT降低中起重要作用,而K+和儿茶酚胺的作用在导致VMRT降低中不起作用。