Hatae J
Jpn J Physiol. 1979;29(1):25-36. doi: 10.2170/jjphysiol.29.25.
The effects of procaine on the contractility of the bullfrog's ventricular muscle were investigated. The addition of 10(-5) g/ml of procaine potentiated the twitch tension which was accompanied by an elevation as well as a prolongation of the action potential plateau. This positive inotropism of procaine was not induced by endogenous catecholamine because a beta-blocking agent did not influence this twitch potentiation. The twitch potentiation was increased in proportion to the external Ca concentration, suggesting the possibility of augmentation of Ca influx during the action potential. In normal Ringer solution, procaine suppressed potassium contracture which was composed of two components: an initial phasic component and a late tonic one. Potassium contracture after perfusion with Ca-free solution was also suppressed by procaine. However, potassium contracture which had been treated previously with La was composed of only a tonic component and was potentiated by procaine in spite of perfusion with Ca-free solution. The tonic component of potassium contracture may be considered to occur with intracellular Ca. Procaine may increase the Ca inward current, acting on the intracellular Ca storage site and consequently accelerate the excitation-contraction coupling in frog ventricular muscle.
研究了普鲁卡因对牛蛙心室肌收缩性的影响。加入10(-5)克/毫升的普鲁卡因可增强抽搐张力，同时伴有动作电位平台期的升高和延长。普鲁卡因的这种正性肌力作用不是由内源性儿茶酚胺诱导的，因为一种β受体阻滞剂不影响这种抽搐增强作用。抽搐增强作用与细胞外钙浓度成比例增加，提示在动作电位期间钙内流增加的可能性。在正常任氏液中，普鲁卡因抑制钾挛缩，钾挛缩由两个成分组成：初始的相性成分和后期的强直性成分。用无钙溶液灌注后的钾挛缩也被普鲁卡因抑制。然而，先前用镧处理过的钾挛缩仅由强直性成分组成，并且尽管用无钙溶液灌注，仍被普鲁卡因增强。钾挛缩的强直性成分可能被认为是细胞内钙引起的。普鲁卡因可能增加钙内向电流，作用于细胞内钙储存部位，从而加速蛙心室肌的兴奋-收缩偶联。
