Characterization of postischemic myocardial oxygen utilization.
To define the pertubations in myocardial oxygen consumption (MVO2) previously noted after potassium-induced arrest, MVO2 was determined in 19 canine hearts during isovolumetric pressure-volume loading before and serially after 2 hr of cardioplegic ischemia at 20 degrees C. Starling curves were initially unchanged after cardioplegic arrest, but postischemic propranolol (0.2 mg/kg) depressed peak developed pressure 36 +/- 4% and heart rate 24 +/- 1% (p less than .01, for both). MVO2 indexed per beat and for left ventricular weight at defined ranges of peak developed pressure was augmented postischemically by 40% (p less than .05) and this increased oxygen utilization persisted after attenuation of coronary hyperemia, normalization of oxygen extraction, 1 hr of reperfusion, and effective beta-adrenergic-receptor blockade. These data suggest that increased MVO2 to generate physiologic pressures is a sensitive biological marker for cardioplegic efficacy that is independent of coronary flow and oxygen uptake and is not solely attributable to increased beta-adrenergic stimulation.
D000818:Animals; D003326:Coronary Circulation; D003327:Coronary Disease / Q000378:metabolism* / Q000503:physiopathology; D004285:Dogs; D006324:Heart Arrest, Induced; D006339:Heart Rate / Q000187:drug effects; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption; D011433:Propranolol / Q000494:pharmacology; D013599:Systole / Q000187:drug effects
D011433:Propranolol