Decreased regional lactate production and output due to intracoronary continuous infusion of esmolol during acute coronary occlusion in dogs.
This study was designed to test the hypothesis that intracoronary administration of esmolol can confer metabolic protection during coronary constriction or occlusion, without affecting hemodynamic parameters, in a canine model. Seventeen anesthetized open-chest dogs underwent direct cannulation of the left anterior descending coronary artery (LADa), its companion vein (LADv), and the distal circumflex vein (CFXv). LADa flow was measured with an electromagnetic flowmeter. Using a micrometer-driven snare around the LADa, flow was reduced by 50%, 75%, and 100% for 15 minutes, with 1 hour of normal flow before each constriction. In 7 dogs (group 1) chosen randomly, esmolol, 15 to 20 micrograms/kg/min, was infused continuously into the LADa; the rate was adjusted to maintain baseline hemodynamic values. The second group (10 dogs) was not treated with esmolol. Heart rate (HR), electrocardiogram (ECG), LADa flow, LV dP/dt, and aorta (Ao), pulmonary artery (PA), LADa, and left ventricular (LV) pressures were recorded continuously. Cardiac output (CO) (thermodilution) was measured and blood was sampled from all catheters before and after constrictions for analysis of glucose, lactate, sodium, potassium, and blood gases. Flow and pressure in the LADa in both groups decreased similarly during each corresponding constriction. Systolic LV pressure, LV dP/dt, and LV stroke work index were affected in both groups only during 100% constriction. HR, Ao, and PA pressures, and total and peripheral pulmonary resistances were affected similarly in both groups during each constriction. Myocardial lactate extraction and consumption were less negative (negative = net production and output) in the LAD perfusion bed during corresponding constrictions with esmolol than without it.(ABSTRACT TRUNCATED AT 250 WORDS)
Department of Anesthesiology, University of Florida College of Medicine, Gainesville.
A
A
Sidi
W
W
Rush
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001794:Blood Pressure / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D003326:Coronary Circulation / Q000187:drug effects; D003327:Coronary Disease / Q000378:metabolism* / Q000503:physiopathology; D004285:Dogs; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D007773:Lactates / Q000097:blood / Q000378:metabolism*; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption / Q000187:drug effects; D011188:Potassium / Q000097:blood; D011412:Propanolamines / Q000494:pharmacology*; D013318:Stroke Volume / Q000187:drug effects; D014655:Vascular Resistance / Q000187:drug effects; D016277:Ventricular Function, Left / Q000187:drug effects
D000319:Adrenergic beta-Antagonists; D001786:Blood Glucose; D007773:Lactates; D011412:Propanolamines; C036604:esmolol; D011188:Potassium; D010100:Oxygen