Ultrasonic backscatter is substantially modified by pathologic changes in myocardium. Influence of physiologic changes in heart rate, mean arterial pressure, preload, and inotropic state were studied in 17 anesthetized open-chest dogs. Heart rate was changed with atrial pacing/ULFS'49 (a selective bradycardiac agent). Mean arterial pressure was varied with aortic constriction/nitroprusside, preload was altered with nitroglycerin/volume infusion, and inotropic states were altered with dobutamine (10 microns/kg)/esmolol (100 microns/kg). IBR5, an optimum weighted frequency average (4 to 6.8 MHz) of the squared envelope of diffraction corrected for absolute backscatter, and the Fourier coefficient of amplitude modulation (FAM), an index of cardiac cycle-dependent variation, were measured from six sequential electrocardiographically gated intervals throughout the cardiac cycle. Heart rate, mean arterial pressure, preload, and inotropic state did not significantly affect IBR5. FAM increased from 3.5 +/- 0.3 dB (mean +/- SEM) to 7.0 +/- 0.4 dB (p less than .01) at a heart rate of 120 beats/min, and decreased to 3.9 +/- 0.4 at a heart rate of 160 beats/min. No change in FAM was noted with a rise (70 +/- 12 to 45 +/- 10 mmHg) in mean arterial pressure or preload (an increase or decrease in diastolic segment length of +/- 10% from the baseline). Dobutamine produced a significant increase in left ventricular dP/dt (2600 +/- 200 to 3475 +/- 275 mm Hg) and FAM (3.4 +/- 0.1 to 6.4; p less than .01). Esmolol significantly reduced left ventricular dP/dt (2600 +/- 200 to 2000 +/- 175 mm Hg, p less than .05) and FAM (3.4 +/- 0.01 to 6.4 +/- 0.1; p less than .01). We conclude that IBR5 is independent of heart rate, mean arterial pressure, preload, and inotropic state. Cardiac cycle-dependent amplitude modulation follows changes in cardiac contraction.