Regional oxygen consumption and supply in heart: Effect of methoxamine-induced pressure rise

The effect of raising arterial blood pressure 50 mmHg with methoxamine on regional left ventricular O₂ supply and consumption was studied in 27 pentobarbital-anesthetized open chest rabbits. Three groups of animals were studied: control, methoxamine infusion sufficient to raise pressure 50 mmHg, and methoxamine infusion sufficient ro raise pressure 50 mmHg with atrial pacing to maintain heart rate. Subepicardial (epi) and subendocardial (endo) O₂ saturations were determined with a microspectrophotometric technique. Regional flow was determined with radioactive microspheres and regional O₂ consumption by the Fick principle. In the control group, endo venous O₂ saturation [31 ± 3% (SE)] was lower than epi (42 ± 2%). There were no significant regional differences in blood flow (avg 128 ± 2 ml.min^-1.100g^-1). With methoxamine when heart rate fell, there were no differences in regional flow or consumption when compared to control. During methoxamine infusion, when heart rate was maintained, there was higher coronary blood flow (361 ± 52 ml.min^-1.100 g^-1) and O₂ consumption (27 ± 4 ml O₂.min^-1.100 g^-1). No regional differences, epi vs. endo, were found in this group. After a 50-mmHg pressure rise, the endo region of the left ventricle had an increased O₂ consumption mediated by an increased coronary blood flow without a significant rise in O₂ extraction, similarly to epi.