Effect of arterial pressure on left ventricular O2 consumption, coronary blood flow, and reserve capacity following coronary occlusion

Abstract

The effect of mean systemic arterial pressure (SAP) on myocardial O2 consumption (MVO2) coronary blood flow (CBF) and the reduction of left ventricular (LV) reserve capacity resulting from coronary artery occlusion was studied in 25 open-chest pentobarbital anesthetized dogs with fixed cardiac output and controlled heart rate (HR) and SAP. In all animals, baseline MVO2 and CBF were obtained and LV reserve capacity was determined by identifying the HR and SAP level which raised mean left atrial pressure to 12 mm. Hg. After uniform placement of a pericoronary snare, the dogs were randomized to five equal groups, and SAP was set at 40, 70 (two groups), 100, and 130 mm. Hg. MVO2 and CBF were redetermined and the coronary artery was ligated in all except one group (70 mm. Hg) which served as sham control. thirty minutes after coronary occlusion, MVO2, CBF, and LV reserve capacity were determined again. Percent of nonperfused myocardium did not differ among groups (27.6 +/- 1%). MVO2 bore a linear relationship to SAP setting wheras CBF bore a curvilinear relationship. Coronary occlusion did not modify these relationships. Significant, but similar decreases in tolerated HR (23.1 +/- 4.7 min.-1) and SAP (41.9 +/- 6.2 mm. Hg) from control values were observed in all four groups regardless of SAP setting. We concluded that the impact of coronary ligation on MVO2, CBF, the loss of functional reserve capacity, and possibly the extent of ischemic injury of the left ventricle, is not modified by afterload changes. However, optimal O2 supply-to-demand ratio appears at SAP of about 100 mm. Hg.