Lillie C, Kobinger W
Naunyn Schmiedebergs Arch Pharmacol. 1984 Dec;328(2):210-3. doi: 10.1007/BF00512075.
The effects of the two "specific bradycardic agents" AQ-A 39 and alinidine on the spontaneous electrical discharge rate of intact guinea-pig sinus node preparations were investigated. At high external K+-concentrations (10.8 and 16.2 mmol/l) the bradycardic effect of the two drugs was diminished or abolished. In contrast, the negative chronotropic effect of the reference compound verapamil ("Ca2+-antagonist") was enhanced. These results show that the bradycardic effects of AQ-A 39 and alinidine are diminished in depolarized preparations, which makes it unlikely that in intact sinus node preparations the mechanism of action is the same as that of "Ca2+-antagonists".
研究了两种“特异性心动过缓药物”AQ - A 39和阿利尼定对完整豚鼠窦房结标本自发电活动速率的影响。在高细胞外钾浓度(10.8和16.2 mmol/L)时,这两种药物的心动过缓作用减弱或消失。相比之下,参比化合物维拉帕米(“钙拮抗剂”)的负性变时作用增强。这些结果表明,在去极化的标本中,AQ - A 39和阿利尼定的心动过缓作用减弱,这使得在完整窦房结标本中其作用机制不太可能与“钙拮抗剂”相同。