Hübner H, Stephan K, Meesmann W, Abendroth R R
Arzneimittelforschung. 1976;26(8):1561-5.
After acute circumscribed myocardial infarction the effects of the beta-sympatholytic agent 1-(indol-4-yl-oxy)-3-isopropyl-amino-propan-2-ol (pindolol; Visken) on hemodynamics and contractility were examined. Hemodynamic changes after application of pindolol are of small extent only. Heart rate shows a rising tendency whereas systolic and diastolic aortic pressure decreases only after higher doses. Left ventricular end-diastolic pressure (LVEDP) does not change remarkably. Cardiac output is reduced by small doses of pindolol and reaches starting values again before the administration of higher doses. Changes of the contractility parameters (dp/dt)max, t-(dp/dtmax, and PEP in the sense of a beta-sympatholysis appear only in the lower range of the doses given. Thus maximum decrease of contractility is 20% measured at (dp/dt)max, which consequently reaches the starting value again. The other contractility parameters change accordingly. These typical dose-response relations between pindolol and contractility parameters are considered to be due to lacking cardiac depressive properties combined with significant so-called positive intrinsic activity. Our results show that no contraindication can be derived from the small influence of pindolol on contractility in acute myocardial infarction.
在急性局限性心肌梗死后，研究了β-交感神经阻滞剂1-(吲哚-4-基-氧基)-3-异丙基氨基-丙醇（吲哚洛尔；心得静）对血流动力学和收缩性的影响。应用吲哚洛尔后的血流动力学变化仅为轻度。心率呈上升趋势，而仅在较高剂量时收缩压和舒张压才降低。左心室舒张末期压力（LVEDP）无明显变化。小剂量吲哚洛尔可降低心输出量，在给予较高剂量前又恢复到起始值。收缩性参数（dp/dt）max、t-(dp/dtmax)和PEP在β-交感神经阻滞意义上的变化仅出现在所给剂量的较低范围内。因此，以（dp/dt）max测量，收缩性的最大降低为20%，随后又恢复到起始值。其他收缩性参数也相应变化。吲哚洛尔与收缩性参数之间的这些典型剂量反应关系被认为是由于缺乏心脏抑制特性并伴有显著的所谓正性内在活性。我们的结果表明，不能因吲哚洛尔对急性心肌梗死收缩性的微小影响而得出禁忌结论。
