Isovolumic relaxation abnormalities have been noted in the ischemic left ventricle, but altered end-diastolic distensibility, as well as the role of right ventricular distention, is debated. Accordingly, left ventricular end-diastolic pressure and myocardial segment length were studied in the open-chest dogs with critical (90% diameter reduction) stenoses on both left anterior descending and circumflex coronary arteries. Regional segment length was measured with ultrasonic crystals placed subendocardially, and ischemia was induced by pacing tachycardia for 3 minutes. Transient vena caval occlusion was done to unload the right ventricle and to produce a series of left ventricular end-diastolic pressure and left ventricular end-diastolic segment length points before and after pacing tachycardia. After pacing tachycardia, left ventricular end-diastolic pressure (9.3 +/- 0.9 to 16.9 +/- 1.5 mm Hg, P less than 0.001) and time constant T of left ventricular isovolumic pressure decline (46 +/- 3 to 60 +/- 5 msec, P less than 0.01) increased, with an increase in left ventricular end-systolic segment length (9.8 +/- 0.3 to 10.5 +/- 0.3 mm, P less than 0.001), and a decrease in fractional shortening (17.6 +/- 1.7 to 14.5 +/- 1.3%, P less than 0.01) in the ischemic region, although right ventricular end-diastolic pressure was unchanged. With vena caval occlusion, right ventricular diastolic pressure fell promptly to near zero, followed by decrease in left ventricular pressure and segment length. In each dog, the left ventricular end-diastolic pressure-end-diastolic segment length relation shifted upward after pacing tachycardia. Pacing tachycardia was performed again in six dogs without stenoses. In this group, fractional shortening was preserved after pacing tachycardia (15.7 +/- 2.3 to 15.3 +/- 2.3%, NS), and left ventricular end-diastolic pressure (9.4 +/- 1.8 to 9.8 +/- 1.8 mm Hg, NS) was unchanged. The left ventricular end-diastolic pressure-segment length relation did not shift upward after pacing tachycardia. These data indicate that extrinsic compression of left ventricle by right ventricle is unlikely to be responsible for the upward shift in this model, and the upward shift in end-diastolic left ventricular pressure-segment length relations, as well as dynamic left ventricular diastolic pressure-segment length, supports the concept that persistent myosin-actin interaction throughout diastole plays an important role in the diastolic abnormalities in this angina physiology model.