Studies on Experimental Coronary Insufficiency : Effects of Intracoronary Administered Catecholamines on Cortonary Circulation, Cardiac Function and Myocardial Metabolism in Dogs with Graded Coronary Constriction

It has been clearly shown in our studies reported previously that a physiological dose of catecholamines (CA) auguments cardiac function, myocardial metabolism and coronary blood flow in normal heart, while deleterious effects are seen in the heart with coronary constriction. These different effects, benefical or deleterious, may be depend on the coronary blood flow (CBF) level. Therefore, this study was designed to establish the interrelationship between the CA effect on myocardial metabolism or cardiac function and CBF level, and to determine the critical CBF level in which CA produces myocardial ischemia. In 48 anesthetized open chest dogs, the main left coronary artery was cannulated with Griggs type cannula. CBF was measured with electromagnetic flow meter, and was reduced to the desired level (CBF 12?88ml/min/100g) by means of graded constriction in the auto-perfused cannula circuit. The hemodynamic and metabolic measurements were performed before and after CBF reduction and following the intracoronary administration of 0.2μg/kg/min of adrenaline (Ad) or 0.4 of noradrenaline (NA) for 5 minutes. (1) Coronary constriction resulted in a slight decrease of mean coronary blood pressure, Max dp/dt of left ventricle, myocardial oxygen consumption (MVO2), coronary arterio-venous difference of lactate (AL), lactate extraction ratio (ΔL/La) and a slight elevation of left ventricular end-diastolic pressure (LVEDP) in proportion to the degree of CBF reduction. Myocardial potassium loss was found to be below CBF 40 ml/min/100g. (2) CA markedly increased Max dP/dt of left ventricle, MVO2, ΔL,ΔL/La, coronary arterio-venous difference of potassium and lowered LVEDP in dogs with CBF over 50 ml/min/lOOg. (3) Both NA and Ad resulted in a significant production of lactate and potassium loss from myocardium, elevation of LVEDP, and infarct like ST elevation (6/12 dogs) or significant ST depression (other 6/12 dogs) in dogs with CBF under 30 ml/min/100g. From these findings, it was suggested that the critical CBF level, in which CA produces myocardial ischemia, might exist between 30 and 50 ml/min/100g, and CA auguments or improves cardiac function and myocardial metabolism in dog hearts with CBF over 50, while accelerets myocardial ischemia in those with CBF under 30 ml/min/100g