• M Böttcher, J Czernin, K Sun, M E Phelps, and H R Schelbert.
• Department of Molecular and Medical Pharmacology, UCLA School of Medicine 90095-6948, USA.
• J. Nucl. Med. 1997 Mar 1; 38 (3): 442-6.

UnlabelledThe beta 1 receptor blockade reduces cardiac work and may thereby lower myocardial blood flow (MBF) at rest. The effect of beta 1 receptor blockade on hyperemic MBF is unknown.MethodsTo evaluate the effect of selective beta 1 receptor blockade on MBF at rest and during dipyridamole induced hyperemia, 10 healthy volunteers (8 men, 2 women, mean age 24 +/- 5 yr) were studied using 13N-ammonia PET (two-compartment model) under control conditions and again during metoprolol (50 mg orally 12 hr and 1 hr before the study).ResultsThe resting rate pressure product (6628 +/- 504 versus 5225 +/- 807) and heart rate (63 +/- 6-54 +/- 5 bpm) declined during metoprolol (p < 0.05). Similarly, heart rate and rate pressure product declined from the baseline dipyridamole study to dipyridamole plus metoprolol (p < 0.05). Resting MBF declined in proportion to cardiac work by approximately 20% from 0.61 +/- 0.09-0.51 +/- 0.10 ml/g/min (p < 0.05). In contrast, hyperemic MBF increased when metoprolol was added to dipyridamole (1.86 +/- 0.27-2.34 +/- 0.45 ml/g/min; p < 0.05). The decrease in resting MBF together with the increase in hyperemic MBF resulted in a significant increase in the myocardial flow reserve during metoprolol (3.14 +/- 0.80-4.61 +/- 0.68; p < 0.01).ConclusionThe beta 1 receptor blockade increases coronary vasodilatory capacity and myocardial flow reserve. However, the mechanisms accounting for this finding remain uncertain.

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