Changes in regional myocardial metabolism during partial stenosis in the presence of coronary vasodilators.
The relation of regional myocardial metabolism to coronary blood flow during pharmacologic flow elevation with dipyridamole was studied in four unsedated dogs. Chronic catheters were implanted in the aorta, left atrium, and coronary sinus at the anterior cardiac vein for determination across the left anterior descending coronary vascular bed of arteriovenous O2 content, glucose, free fatty acids, and lactate. A flowmeter and inflatable occluder were placed on the left anterior descending coronary artery, and mean aortic pressure and heart rate were recorded. Flow was increased with dipyridamole (0.4 mg/kg i.v.) and subsequently lowered by a partial stenosis in order to examine effects of relative flow decrease on metabolism without reducing flow below resting control or producing ischemia. Regional metabolism was compared at maximum flow and at submaximal flow with partial stenosis. Resting flow, maximal flow, and submaximal flow values were 72 +/- 3, 231 +/- 12, and 121 +/- 10 ml/min/100 g, respectively. When flow was lowered from maximal to submaximal levels, there was a significant decrease in both MVO2, from 8.2 +/- 0.7 to 6.4 +/- 0.5 ml/min/100 g, and free fatty acid uptake, from 23.9 +/- 5.5 to 6.8 +/- 1.0 muEq/min/100 g, p less than 0.01. There was no significant change in glucose uptake, lactate uptake, or external work (heart rate-pressure product). These results demonstrate that coronary blood flow and/or distal coronary pressure is a primary determinant of myocardial metabolism in the absence of changes in external metabolic demand, ischemia, or shifts in substrate utilization. We suggest that this phenomena accounts for the relative infrequency of anginal pain in the presence of perfusion defects during diagnostic imaging.
D000818:Animals; D003326:Coronary Circulation / Q000187:drug effects; D003327:Coronary Disease / Q000378:metabolism*; D004176:Dipyridamole / Q000494:pharmacology; D004285:Dogs; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D007773:Lactates / Q000378:metabolism; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology*
D005230:Fatty Acids, Nonesterified; D007773:Lactates; D014665:Vasodilator Agents; D004176:Dipyridamole; D005947:Glucose