Salzmann R, Scholtysik G, Clark B, Berthold R
J Cardiovasc Pharmacol. 1986 Sep-Oct;8(5):1035-43. doi: 10.1097/00005344-198609000-00023.
DPI 201-106 (4-[3-(4-diphenylmethyl-1-piperazinyl)-2-hydroxypropoxy]-1H-indole -2- carbonitrile) is characterized by a marked cardiotonic activity. The compound exerted positive inotropic effects in anesthetized and conscious dogs, pithed open-chest cats, and isolated hearts of cardiomyopathic hamsters and vanadate-treated guinea-pig atria. Left ventricular dP/dtmax was increased in anesthetized dogs after i.v. injection of 0.2 and 2 mg/kg DPI 201-106 (34 +/- 6 and 104 +/- 18%, respectively) and in unanesthetized dogs after oral doses of 2-8 mg/kg (22 +/- 3 to 50 +/- 5%, respectively). In most experiments, the compound lowered blood pressure and heart rate. Stroke work and left ventricular work were almost unaffected by DPI 201-106, and oxygen consumption and cardiac efficiency remained unchanged in open-chest dogs. Studies of the mechanism of action of DPI 201-106 lead to the conclusion that its positive inotropic effect is not explainable either by beta-stimulation or by liberation of catecholamines. This was shown in anesthetized dogs and pithed open-chest cats pretreated with propranolol and reserpine.
DPI 201 - 106（4 - [3 - (4 - 二苯基甲基 - 1 - 哌嗪基)-2 - 羟基丙氧基]-1H - 吲哚 - 2 - 腈）具有显著的强心活性。该化合物在麻醉和清醒犬、去脑开胸猫以及心肌病仓鼠和钒酸盐处理的豚鼠心房的离体心脏中均表现出正性肌力作用。静脉注射0.2和2mg/kg DPI 201 - 106后，麻醉犬的左心室dp/dtmax增加（分别为34±6%和104±18%），口服2 - 8mg/kg后，未麻醉犬的左心室dp/dtmax也增加（分别为22±3%至50±5%）。在大多数实验中，该化合物会降低血压和心率。DPI 201 - 106对每搏功和左心室功几乎没有影响，在开胸犬中，氧耗量和心脏效率保持不变。对DPI 201 - 106作用机制的研究得出结论，其正性肌力作用既不能用β - 刺激也不能用儿茶酚胺的释放来解释。这在预先用普萘洛尔和利血平处理的麻醉犬和去脑开胸猫中得到了证实。
