Spear J F, Moore E N
J Cardiovasc Pharmacol. 1984 May-Jun;6(3):506-10. doi: 10.1097/00005344-198405000-00020.
To evaluate timolol's ability to antagonize the "slow response" in cardiac tissues, isolated canine cardiac Purkinje fibers were exposed to 0.25 mM barium chloride to induce membrane depolarization, spontaneous automaticity, and slow response action potentials. The effects of timolol on action potential parameters and the cycle length of spontaneous automaticity were tested at concentrations of 10, 100, and 500 micrograms/ml. Timolol significantly depressed the action potential and slowed automaticity only at 100 and 500 micrograms/ml but not at 10 micrograms/ml. Since verapamil and nifedipine have been reported to completely suppress activity in this model at concentrations of 0.2-2.0 micrograms/ml, we conclude that timolol has little direct slow response blocking potency.
为评估噻吗洛尔拮抗心脏组织中“慢反应”的能力,将离体犬心脏浦肯野纤维暴露于0.25 mM氯化钡中,以诱导膜去极化、自发自律性和慢反应动作电位。在10、100和500微克/毫升的浓度下测试了噻吗洛尔对动作电位参数和自发自律性周期长度的影响。噻吗洛尔仅在100和500微克/毫升时显著降低动作电位并减慢自律性,而在10微克/毫升时则无此作用。由于据报道维拉帕米和硝苯地平在0.2 - 2.0微克/毫升的浓度下可完全抑制该模型中的活性,我们得出结论,噻吗洛尔几乎没有直接的慢反应阻断效力。