A B S T R A n .Left ventricular dysfunction has been observed in human infants with pulmonary hypertension. The purpose of this study was to establish whether mechanically increased right ventricular afterload alters left ventricular performance by altering its contractility, configuration, or both. Six neonatal 3-to 7-d-old lambs were acutely instrumented with micromanometer-tipped catheters and two pairs of ultrasonic crystals to measure left ventricular pressure and anterior-posterior and septal-free wall dimensions. The product of these two dimensions, denoted left ventricular area, was used a s an index of left ventricular volume. TWO levels of mechanically increased right ventricular afterload were induced with a closed pericardium under three levels of left ventricular preload produced by whole-blood transfusions. Four brief increases in left ventricular afterload were induced by constricting the aorta under each right ventricular afterload and preload condition. Using multiple linear regression, we found that the slope of the end-systolic pressure-area relationship, an index of contractility, was unchanged 10.90 + 0.1 1 mm Hg/ mm2 (SEM)], and stroke area (65.8 f 7 mm2) and cardiac output (the product of stroke area and heart rate) (13 400 f 1 6 6 0 mm2/min) were maintained. However, the area intercept of the pressure-area line at zero pressure (499 f 13 mm2) shifted significantly to the left in the presence of both levels of increased right ventricular afterload (by 3 5 structurally and functionally immature compared with adult myocardium (1. 2), yet the resting indices of fetal myocardial performanct. al-e ielaiii;eij; high comi ;a:ed :.:i?h those nf ?he rdu!? (3. 4). Because the newborn heart is already functioning near maximum contractility with little further reserve (5-9), direct ventricular interaction may play a more important role in allowing the left ventricle to respond to changes in loading conditions than it does in adults. The intraventricular septum is more compliant in neonates than in fetuses. increasing the potential for direct mechanical interaction between the right and left heart (10). Some infants with persistent pulmonary hypertension of the newborn exhibit left ventricular dysfunction ( 1 1-14). Similarly. adults with acute pulmonary hypertension secondary to acute respiratory failure or cor pulmonale secondary to chronic lung disease have associated left ventricular dysfunction ( 15-17). Ventricular interaction may be partially responsible for this association (18-21). The purpose of this study was to establish whether mechanically increased right ventricular afterload alters left ventricular performance by altering its contractility, configuration (via direct ventricular interaction). or both in the neonate.In a previous study. we demonstrated that mechanically increased right ventricular afterload diminishes left ventricular performance based on simultaneous changes in systemic blood flow and LV dP/dt,,, (22). In contrast. when comparable increased right ventricular afterload wa...