Variations in left ventricular volume alter myocardial oxygen consumption more at low than at high inotropy

Variations in left ventricular (LV) wall tension during changes in LV end‐diastolic volume significantly affect myocardial oxygen consumption (M V O 2 ). In the present study we examined if the reduction in M V O 2 ) per beat accompanying a decline in LV end‐diastolic volume at constant LV systolic pressure (LVSP) is dependent on the level of myocardial inotropy. In six anaesthetized open‐chest pigs, the blood volume was expanded by i. v. infusion of a Ringer solution. At constant heart rate (by atrial pacing) and LVSP (by adjustments of a proximal aortic snare), LV end‐diastolic volume was reduced in steps by withdrawals of blood. This procedure was performed at high inotropy (during a continuous intracoronary infusion of isoproterenol, 0.40 ± 0.08 μg min ‐1 ), and at low inotropy (after i. v. injection of 3.4 ± 0.2 mg propranolol). LVSP was about 25 mmHg higher at high than at low inotropy. The fall in LV tension was therefore greater during blood volume reductions at high than at low inotropy because the fall in LV end‐diastolic volume was almost identical and was initiated from the same level at both high and low inotropy. Nevertheless, the slope of the M V O 2 /LV end‐diastolic volume relationship was significantly ( P < 0.05) less steep at high (1.26 ± 0.30 μmol 100 g ‐1 mm ‐1 ) than at low inotropy (2.06 ± 0.48 μmol 100 g ‐1 mm ‐1 ). M V O 2 per beat fell by only 0.79 ± 0.17 μmol 100 g ‐1 (from 6.03 ± 0–4±5 μmol 100 g ‐1 = 13.8 ± 3.1%) at high inotropy compared with 1.21 ± 0.19 μmol 100 g ‐1 (from 3.79 ± 0.29 μmmol 100 g ‐1 = 30.5 ± 3.4%) at low inotropy. The greater reduction in M V O 2 per beat at low inotropy was associated with a reduction in LVd P /d t of 24 ± 4%, whereas LVd P /d t remained unchanged at high inotropy. Thus, the changes in M V O 2 per beat and LVd P /d t were closely correlated ( r = 0.94), and because the reduction in contractility was present only after propranolol administration it appeared to be induced by mechanisms other than variations in β‐adrenergic stimulation.