Characterization of postischemic myocardial oxygen utilization

KRUKENKAMP, IRVIN B. M.D.
SILVERMAN, NORMAN A. M.D.
SORLIE, DAG M.D.
PRIDJIAN, ARA M.D.
FEINBERG, HAROLD PHD.
LEVITSKY, SIDNEY M.D.

Departments of Surgery and Pharmacology, University of Illinois College of Medicine at Chicago.

Address for correspondence: Norman A. Silverman, M.D., Department of Surgery, P.O. Box 6998, Chicago, IL 60680. Presented in part at the 58th Annual Scientific Sessions of the American Heart Association, Washington, D.C., November 13, 1985.

Received August 2, 1994; revision accepted September 23, 1994.

Circulation 74:p III-129, November 1986.

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 200 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 < .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 < .05) and this increased oxygen utilization persisted after attenuation of coronary hyperemia, normalization of oxygen extraction, 1 hr of reperfusion, and effective 13-adrenergicreceptor 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 3-adrenergic stimulation.