Bonandi L, Metra M, Niccoli L, Ettori F, Nodari S, Dei Cas L, Visioli O
Cattedra di Cardiologia, University of Brescia, Italy.
Cardiovasc Drugs Ther. 1992 Oct;6(5):513-7. doi: 10.1007/BF00055610.
Cicloprolol is a new beta-blocking agent with high selectivity for beta 1 receptors and high intrinsic sympathomimetic activity. We studied the acute hemodynamic effects of cicloprolol in nine subjects with no evidence of left ventricular dysfunction who underwent cardiac catheterization for the evaluation of chest pain. All patients had normal coronary angiography and left ventriculography. Left ventricular pressure was determined throughout the cardiac cycle using a Millar 8Fr Minotip catheter; an echocardiogram, phonocardiogram, and ECG were simultaneously recorded to obtain left ventricular pressure-diameter loops. All the measurements were repeated before and after the intravenous administration of cicloprolol. Cicloprolol was administered at increasing doses of 0.05, 0.10, and 0.25 mg/kg until a cardiac output increase of at least 15% over basal values was achieved. A decrease of mean arterial pressure or cardiac output after cicloprolol was not observed in any patient. Cicloprolol administration significantly increased cardiac output (24%), stroke volume (22%), and peak positive dP/dt (25%); no significant changes in heart rate, systemic blood pressure, right atrial pressure, or pulmonary artery pressures were observed. No significant change in the echocardiographic parameters occurred. Among the indices of left ventricular diastolic function, the time constant of isovolumetric relaxation was significantly decreased (-43%) after cicloprolol; moreover, the left ventricular pressure-diameter loop in the protodiastolic phase was shifted to the left following cicloprolol infusion. This study confirms that in subjects with normal left ventricular function cicloprolol can improve resting left ventricular systolic function, and it shows that this action can also be attended by a more rapid isovolumetric relaxation, similar to what has been observed with other sympathomimetic amines.
环丙洛尔是一种对β1受体具有高选择性且具有高内在拟交感活性的新型β受体阻滞剂。我们研究了环丙洛尔对9名无左心室功能障碍证据且因胸痛接受心导管检查的受试者的急性血流动力学影响。所有患者冠状动脉造影和左心室造影均正常。使用Millar 8Fr微型尖端导管在整个心动周期中测定左心室压力;同时记录超声心动图、心音图和心电图以获得左心室压力-直径环。在静脉注射环丙洛尔前后重复所有测量。以0.05、0.10和0.25mg/kg递增剂量给予环丙洛尔,直至心输出量比基础值增加至少15%。在任何患者中均未观察到环丙洛尔后平均动脉压或心输出量降低。给予环丙洛尔后心输出量显著增加(24%)、每搏量增加(22%)和峰值正dP/dt增加(25%);未观察到心率、体循环血压、右心房压力或肺动脉压力有显著变化。超声心动图参数无显著变化。在左心室舒张功能指标中,环丙洛尔后等容舒张时间常数显著降低(-43%);此外,输注环丙洛尔后舒张前期的左心室压力-直径环向左移位。本研究证实,在左心室功能正常的受试者中,环丙洛尔可改善静息时左心室收缩功能,并且表明这种作用还可伴有更快的等容舒张,类似于其他拟交感胺所观察到的情况。