Purfürst W D, Günther K H, Hujer W, Siewert H, Strangfeld D
Z Kardiol. 1986 Aug;75(8):489-95.
Exercise investigations were performed in 39 male hypertensives (WHO stage I-III) to assess haemodynamics and cardiac function after intravenous application of 5 mg propranolol for the detection of latent heart failure. Radiocardiography was used to determine volumetric parameters such as LV end-diastolic volume and ejection fraction, and microcatheterization was employed to obtain the LV filling pressure via pressure measurement in the pulmonary artery (PA). The negative inotropic and chronotropic effects of propranolol on pump function and myocardial mechanics at rest were found to be minimal. During 50 watt exercise however, an increase of the diastolic PA pressure has been observed simultaneously with a diminution of cardiac output (stroke volume being constant). Thus, under acutely administered beta blockade, a general disturbance in the flow-pressure relation could be induced, being comparable to heart failure. Only in a few cases was the reduced contractility compensated by the Frank-Starling mechanism, but only if the mechanism did not participate in the regulation of pump function during the previous control investigation. In other cases a remarkable reduction of cardiac output and even stroke volume occurred, results which may be explained as a consequence of a reduced venous return (or pooling) connected with acutely induced vascular effects (beta-2 blockade).
对39名男性高血压患者(世界卫生组织I - III期)进行了运动研究,以评估静脉注射5毫克普萘洛尔后检测潜在心力衰竭时的血流动力学和心脏功能。采用放射心动图测定左心室舒张末期容积和射血分数等容积参数,并通过肺动脉压力测量使用微导管插入术获取左心室充盈压。发现普萘洛尔对静息时泵功能和心肌力学的负性肌力和负性变时作用极小。然而,在50瓦运动期间,观察到舒张压肺动脉压升高,同时心输出量减少(每搏量恒定)。因此,在急性给予β受体阻滞剂的情况下,可诱发血流 - 压力关系的普遍紊乱,类似于心力衰竭。只有少数情况下,Frank - Starling机制可代偿收缩力降低,但前提是该机制在前一次对照研究中未参与泵功能的调节。在其他情况下,心输出量甚至每搏量显著降低,这些结果可解释为与急性诱导的血管效应(β2受体阻滞)相关的静脉回流减少(或淤积)的结果。