Hamada K, Yamazaki J, Nagao T
Laboratory of Pharmacology and Toxicology, Graduate School of Pharmaceutical Sciences, University of Tokyo, Japan.
Jpn J Pharmacol. 2001 Jun;86(2):251-3. doi: 10.1254/jjp.86.251.
The purpose of the following experiment was to determine whether amelioration of myocardial contractile dysfunction by diltiazem is mediated by shortening of monophasic action potential duration (MAPD) during myocardial ischemia in anesthetized dogs. Diltiazem improved regional contraction during reperfusion after 10-min occlusion. The shortening of MAPD and increase in [K+]e were blunted by treatment with diltiazem. These results suggest that shortening of action potential duration during myocardial ischemia is unlikely to be a reason for the amelioration of contractile dysfunction.
以下实验的目的是确定在麻醉犬心肌缺血期间,地尔硫䓬改善心肌收缩功能障碍是否是通过缩短单相动作电位持续时间(MAPD)来介导的。在10分钟阻断后再灌注期间,地尔硫䓬改善了局部收缩。地尔硫䓬治疗可减弱MAPD的缩短和细胞外钾离子浓度([K+]e)的升高。这些结果表明,心肌缺血期间动作电位持续时间的缩短不太可能是收缩功能障碍改善的原因。