Coronary and myocardial actions of the antianginal drugs, papaverine and prenylamine were significantly altered by selective blockade of the adrenergic β receptors both in the heart in situ as well as in the isolated fibrillating heart. In the intact anesthetized dog the coronary vasodilating action of 0.5 mg/kg i.v. papaverine and 1.0 mg/kg i.v. prenylamine as well as their effect in increasing coronary flow (coronary sinus outflow and myocardial 'nutritive' blood flow) was considerably depressed by the blockade of the adrenergic β receptors, induced by pronethalol (2 mg/kg i.v.) and propranolol (0.5 mg/kg i.v.) respectively. The effect of papaverine in increasing myocardial O2 consumption was reversed by the blockade, whereas the effect of prenylamine itself which reduced somewhat the myocardial O2 uptake was even more marked after pronethalol treatment. Similar results concerning the papaverine and prenylamine effect on O2 consumption were obtained in the isolated fibrillating dog heart perfused with a constant volume of blood from a donor animal, but the vasodilating action of the drugs increased in this preparation after blockade of the adrenergic β receptors. Possible causes of this discrepancy between the results obtained in the isolated heart and in the heart in situ are discussed. On the basis of our findings an adrenergic mechanism acting at the β receptor sites seems to at least partly responsible for the action of the antianginal drugs used in causing coronary vasodilation, and increasing metabolic rate and coronary flow. The action of papaverine in improving myocardial oxygenation (O2 supply/O2 demand) was increased by blockade of the adrenergic β receptors, an increase which was less marked for prenylamine.
- Adrenergic β receptor blockade
- Papaverine Myocardial 'nutritive' blood flow
- Prenylamine Constant flow thermodilution
- Pronethalol Coronary dilating action
- Propranolol Myocardial O consumption
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