Coronary vasodilation produced by tachycardia under various basal flow conditions.

Some properties of coronary vasodilation produced by heart rate elevation under various basal coronary flow levels was studied. Coronary sinus blood flow, myocardial oxygen consumption and left ventricular contractile force were measured in anaesthetized, open-chest dogs. Heart rate was progressively increased by electrical stimulation at rates ranging from 60/min to 210/min. This was repeated during control, noradrenaline infusion (0.2 microgram kg-1 min-1), in the presence of propranolol (0.25 mg/kg), and during hypopneic positive pressure respiration. It was found that under all experimental conditions, coronary perfusion increased linearly with heart rate. At each rate, coronary flow was greater during noradrenaline infusion and hypopneic respiration than that observed during control or following beta-blockade. Myocardial oxygen consumption behaved similarly to flow, and MVO2 was lowest in the presence of propranolol, and highest during hypopneic ventilation and catecholamine infusion. Contractile force per min (heart rate x tension) also increased with increasing heart rate, but was greatest during noradrenaline infusion, lowest during beta-blockade, and similar during both control and hypopneic respiration. These results indicate that the oxygen cost of contraction was different under the various conditions, and was particularly wasteful during hypopneic respiration. It is concluded that autoregulation caused by heart rate elevation is not dependent on the initial state of coronary blood flow, and that endogenous catecholamine release cannot account for this phenomenon.