The conundrum of the effect of beta-blockade on myocardial oxygen consumption

The effect of propranolol on myocardial oxygen consumption was studied in in situ canine hearts. In 12 afterload independent isovolumic hearts propranolol increased MVO2 an average of 19 +/- 3% (P less than 0.01) for all peaked developed pressure intervals from 75 to 175 mm Hg, secondary to increased wall stress. In 10 hearts instrumented for computer acquisition of pressure-volume workloops during progressive volume loading on right heart bypass, propranolol decreased preload recruitable stroke work an average of 36% (P less than 0.05). However, propranolol failed to decrease the amount of oxygen consumed for basal metabolism or external mechanical work when MVO2 is indexed for heart rate, heart weight, and stroke work. Therefore, propranolol does not decrease MVO2 for individual contractions and does not affect the energy requirements for basal metabolism, excitation-contraction coupling, and heat generation, in contrast to results obtained with beta agonists.