Does beta-blockade directly reduce myocardial oxygen consumption?
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%).
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000818:Animals; D001262:Atenolol / Q000494:pharmacology; D001285:Atropine / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects; D004285:Dogs; D006321:Heart / Q000187:drug effects; D006339:Heart Rate / Q000187:drug effects; D009206:Myocardium / Q000378:metabolism*; D009599:Nitroprusside / Q000494:pharmacology; D010101:Oxygen Consumption / Q000187:drug effects*; D010869:Pindolol / Q000494:pharmacology; D011412:Propanolamines / Q000494:pharmacology
D000319:Adrenergic beta-Antagonists; D011412:Propanolamines; D009599:Nitroprusside; D001262:Atenolol; D001285:Atropine; D010869:Pindolol; C025716:ICI 89406