Role of preload and inotropy in stroke volume regulation at constant heart rate.

The relationship between preload and inotropy on left ventricular function was studied in anaesthetized open-chest dogs, by measuring left ventricular dimensions and stroke volume before and during saline infusion at different levels of inotropy. Left ventricular dimensions were continuously estimated by recording myocardial chord length (MCL) in the anterior wall of the left ventricle by ultrasonic technique. The effects of isoproterenol, a stimulator of adrenergic beta-receptors (high inotropy), and propranolol, an inhibitor of adrenergic beta-receptors (low inotropy), were examined during right atrial pacing at constant heart rate averaging 161 +/- 5 beats/min. Stroke volume was varied within the range 9.0 +/- 1.7 ml to 28.6 +/- 3.2 ml by increasing inotropy and preload. To increase preload, saline was infused intravenously until end-diastolic MCL increased by about 10% and left ventricular end-diastolic pressure was higher than 10 mmHg. At constant heart rate and blood volume, both before and during saline infusion, end-diastolic MCL was not influenced by isoproterenol or propranolol administration. End-systolic MCL was reduced by raising inotropy. The difference between end-diastolic and end-systolic MCL, the systolic myocardial shortening (MS), increased during saline infusion; the relative increase in MS was the same at high and low inotropy. On average, MS was more than 50% longer at high than at low inotropy, both before and after saline infusion. Thus, left ventricular end-diastolic volume is increased by saline infusion and end-systolic volume is reduced by increasing inotropy. Preload and inotropy exert independent effects on stroke volume.