To examine the cardiovascular response to prostaglandin E1 infusion, we observed hemodynamic changes including left ventricular diameter (an ultrasonic crystal pair) during PGE(1)-induced hypotension in anesthetized open-chest dogs. Left ventricular contractility was assessed primarily by measuring the slope of the left ventricular endsystolic pressure-diameter relation (ESPDR) determined by combining end-systolic points from a vena caval occlusion. The cardiovascular effects of induced hypotension by infusions of trinitroglycerin and adenosine triphosphate were also examined at the equivalent magnitude of hypotension. Approximately 25% reduction of systemic blood pressure was produced by the three agents. PGE(1) significantly increased cardiac output from 1200 +/- 132 to 1439 +/- 162 ml.min(-1) (mean +/- SE, P < 0.05), stroke volume from 9.1 +/- 1.1 to 10.0 +/- 1.0 ml (P < 0.05), and %-diameter shortening from 10.4 +/- 0.8 to 14.4 +/- 0.8% ( P < 0.01), but the slope of ESPDR was unchanged. Similar changes were also observed during adenosine triphosphate-induced hypotension. PGE(1) significantly decreased end-diastolic diameter in a similar manner to trinitroglycerin. Thus PGE(1) appears to have little influence on left ventricular contractility aside from its effects on afterload and preload, indicating that it is a useful agent for producing controlled hypotension during anesthesia.