Reversible aortic insufficiency was produced in six dogs before and during aortic contrictions at control myocardial inotropy, during high and low inotropy induced by calcium infusion and propranolol administration, respectively. Myocardial chord lengths (MCL) of the left ventricular wall were continuously recorded by ultrasonic technique. Activation of the Frank-Starling mechanism during aortic insufficiency was verified by an increase in end-diastolic length and systolic shortening of MCL. Efficiency of the Frank-Starling mechanism was calculated as the quotient between the rise in systolic shortening and the rise in end-diastolic MCL. At control blood pressure, the efficiency of the Frank-Starling mechanism was 59 +/- 3, 76 +/- 6 and 53 +/- 6% at control, high and low inotropy, respectively. After raising systolic ventricular pressure 30-40 mmHg by aortic constriction, the efficiency of the Frank-Starling mechanism decreased at control inotropy to 41 +/- 7 and at low inotropy to 32 +/- 9% but did not decrease significantly at high inotropy (70 +/- 6%). During periods with aortic insufficiency, left ventricular afterload is increased and it is concluded that the apparent greater efficiency of the Frank-Starling mechanism at high than at low inotropy. At either level of inotropy and afterload examined and at constant heart rate, the Frank-Starling mechanism was activated on a beat to beat basis.