Is reduced cardiac performance the only mechanism for myocardial infarct size reduction during beta adrenergic blockade?

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Abstract
Equal reductions in heart rate (44 beats·min−1) were obtained in cats by treatment with either the beta blocking agent timolol or alinidine, an agent claimed to cause bradycardia without interfering with beta adrenoceptor function. Infarct size was measured by staining with triphenyl-tetrazolium-chloride after 5 h of coronary occlusion and related to the area of hypoperfused myocardium as measured by autoradiography. Regional myocardial blood flow was measured by 15 μm radiolabelled microspheres. Compared with the control cats, in whom 87.4 (SEM2.2)% of hypoperfused myocardium developed into necrosis, timolol reduced infarct size to 65.8 (SEM 2.6)% (p<0.001) and alinidine to 76.2 (SEM 3.1)% (p<0.01) of the hypoperfused area. Timolol reduced infarct size more than did alinidine (p<0.01). Necrosis was more extensive in the endocardium than in the epicardium in all groups. In the subendocardium timolol and alinidine reduced infarct size to the same extent, whereas timolol reduced infarct size more than alinidine in the subepicardium. Although heart rate proved to be the dominant haemodynamic predictor of infarct size, this study indicates that mechanisms other than reduced oxygen demand associated with bradycardia and cardiodepression are operating in the ischaemic myocardium during beta adrenergic blockade.