Shudo I, Saito H, Tanabe T
Jpn J Pharmacol. 1975 Dec;25(6):639-43. doi: 10.1254/jjp.25.639.
The action of ouabain on myocardial inotropism pretreated with 6-hydroxydopamine and alpha-methyl-p-tyrosine was studied. Inotropic action of ouabain was not changed by depletion of catecholamines in the brain, in which the central sympathetic neurons were destroyed by an intraventricular administration of 6-hydroxydopamine. Systemic administration of 6-hydroxydopamine and alpha-methyl-p-tyrosine reduced ventricular catecholamines to 5.3% and 20.8% of the control, respectively. Percent increase of contractility by ouabain after the pretreatment of 6-hydroxydopamine and alpha-methyl-p-tyrosine was reduced to 16.7% and 50.3% of the control, respectively. The results obtained suggest that catecholamines in the myocardium play some important role in producing cardiotonic action of cardiac glycosides. Brain catecholamines or the central sympathetic nervous system do not appear to participate in the exertion of the positive inotropic action of cardiac glycosides.
研究了哇巴因对用6-羟基多巴胺和α-甲基-对-酪氨酸预处理的心肌变力作用。通过脑室内注射6-羟基多巴胺破坏中枢交感神经元，使脑内儿茶酚胺耗竭，并未改变哇巴因的变力作用。全身给予6-羟基多巴胺和α-甲基-对-酪氨酸后，心室儿茶酚胺分别降至对照值的5.3%和20.8%。用6-羟基多巴胺和α-甲基-对-酪氨酸预处理后，哇巴因使收缩性增加的百分比分别降至对照值的16.7%和50.3%。所得结果提示，心肌中的儿茶酚胺在强心苷产生强心作用中起重要作用。脑内儿茶酚胺或中枢交感神经系统似乎不参与强心苷正性变力作用的发挥。
