Effect of left ventricular (LV) volume on right ventricular (RV) end-systolic pressure-volume relation (ESPVR) was investigated, and the mechanism was examined from a standpoint of the alteration of RV free wall mean fiber length. Twelve cross-circulated isovolumically contracting canine hearts in which both ventricular volumes were controlled independently were used, and RV-ESPVR was determined at three different LV volume levels. At small (10.2 ± 0.6 ml), middle (IS J ± 1.0 ml), and large (20.5 ± 1.4 ml) LV volume, the slope of the RV-ESPVR was 2.63 ± 0.13, 2.74 ± 0.13, and 2.89 ± 0.12 mm Hg/ml, respectively, and each value was significantly different from the others (p<0.01). The volume intercept (V0) of the relation (RV-V0) was significantly decreased with the increment of LV volume (RV-V0 in small, middle, and large LV volume; 3.92 ± 0.68, 3.39 ± 0.67, and 2.87 ± 0.71 ml, respectively;p<0.01). In nine hearts, RV free wall lengths in latitudinal and meridional direction were measured at three LV volume levels when RV volume was held constant (16.1 ± 1.1 ml). RV latitudinal end-diastolic length was significantly augmented with increasing LV volume (latitudinal length in small, middle, and large LV volume; 9.68 ± 0.55, 9.81 ± 0.56, and 9.92 ± 0.55 mm, respectively). RV meridional end-diastolic length also increased significantly with increasing LV volume. We concluded that RV-ESPVR showed upward-leftward shift with increasing LV volume and that this shift could be, at least in part, explained by the alteration of end-diastolic length in RV free wall that occurred with constant RV volume (resetting of regional preload), probably due to the deformation of RV becoming more crescent.