Thomas M, Gabe I T, Kimber H, Mills C J, Sweeting T J
Cardiovasc Res. 1981 May;15(5):254-61. doi: 10.1093/cvr/15.5.254.
This paper describes a method for determining whether beta-blocking agents reduce myocardial oxygen consumption by a direct action on the myocardium in addition to that reduction produced by changes in cardiac mechanical function. Measurements of myocardial oxygen consumption were made in anaesthetized dogs . Changes in heart rate were produced by atropine and by ventricular pacing. Alterations in ventricular loading were achieved by balloon inflations in the descending aorta and by infusions of nitroprusside and dextran. Measurements under these conditions were repeated after beta-blockade. Analysis required the separation of the part of reduced myocardial oxygen consumption resulting from the mechanical effects of beta-blockade from any possible additional direct effect on the myocardium. There was no evidence for a significant direct effect. The average overall reduction in myocardial oxygen consumption after beta-blockade was 18% but the estimated reduction not accountable to mechanical effects was only 2% (range, 95% probability, -7% to 3%).
本文描述了一种方法，用于确定β受体阻滞剂除了通过改变心脏机械功能来降低心肌耗氧量外，是否还通过对心肌的直接作用来降低心肌耗氧量。在麻醉犬身上测量心肌耗氧量。通过阿托品和心室起搏来改变心率。通过降主动脉内气囊充气以及输注硝普钠和右旋糖酐来改变心室负荷。在β受体阻滞剂阻断后，重复在这些条件下的测量。分析需要将β受体阻滞剂的机械效应导致的心肌耗氧量降低部分，与对心肌任何可能的额外直接效应区分开来。没有证据表明存在显著的直接效应。β受体阻滞剂阻断后，心肌耗氧量的平均总体降低为18%，但估计无法归因于机械效应的降低仅为2%（范围，95%概率，-7%至3%）。
