CORONARY REACTIONS TO CARDIAC HYPERACTIVITY AND TO HYPOXIA IN ISOLATED PERFUSED HEART OF RAT

1 Continuous recording of cardiac force of contraction, heart rate and coronary flow from isolated perfused hearts of rats was used to study coronary reactions: (a) to cardiostimulation with noradrenaline, CaCl 2 , or electrically induced tachycardia; (b) to short duration stoppage of coronary inflow (hypoxia). 2 The heart rate was controlled by electrical pacing. Coronary vasodilatation resulted from cardiostimulation or hypoxia. This coronary response was greater at higher heart rates. 3 In parallel experiments administration of noradrenaline to hearts paced at different frequencies resulted in a rate‐dependent elevation of adenosine‐3′,5′‐cyclic monophosphate (cyclic AMP). 4 Duration of hypoxia leading to different degrees of reactive hyperaemia did not change the cardiac cyclic AMP levels. 5 Coronary vasodilatation due to increased cardiac metabolism produced by noradrenaline, Ca 2+ or tachycardia was enhanced by the phosphodiesterase inhibitors diazoxide and papaverine while it was inhibited during the administration of prostaglandin E 2 . 6 Reactive hyperaemia was unaffected by diazoxide, papaverine or prostaglandin E 2 . 7 Catecholamine depletion by reserpine did not influence metabolic coronary dilatation nor the reactive hyperaemic responses. 8 We postulate that there are at least two types of coronary reactions: one in response to hypoxia, ‘reactive hyperaemia’, and another resulting from cardiac hyperactivity, ‘metabolic coronary dilatation’. The latter, blocked by prostaglandin E 2 and enhanced by diazoxide or papaverine, would be triggered by cyclic AMP while reactive hyperaemia would result from other mechanisms.