Norepinephrine (NE) infused into the left coronary artery (LCA) of fetal lambs to achieve myocardial concentrations similar to those observed in blood during acute fetal hypoxemia, increases heart rate (HR) and left ventricular output (LVO) without affecting arterial pressure. Infusion into the LCA reaches the LV and septum, but not the RV free wall. We examined the effect of NE infusion into the LCA on LV and RV performance and output in 7 chronically instrumented fetal lambs (gest. age 126-132 d). Aortic (Ao) and pulmonary (PA) ultrasonic flow transducers were implanted to record LVO and RVO. LV and RV contractility were assessed from peak velocity and flow acceleration (dV/dt max). A catheter was inserted into a small branch of the LCA, close to its origin for infusion; NE was infused in amounts of 0.02 μg/min. HR increased from 167 ± 26 to 213 ± 49/min (p < 0.05). LVO rose from 380± 153 to 431 ± 135 ml/min (p < 0.03) and RVO from 498± 170 to 547 ± 250 ml/min (p 0.18). Neither LV nor RV stroke volume (SV) changed significantly. Ao peak flow increased from 1.76 ± 0.24 to 2.01 ± 0.25 L/min (p < 0.001) and Ao dV/dt max rose from 1046 ± 248 to 1496 ± 352 ml/sec/sec (p < 0.005). In contrast PA peak flow (2.04 ± 0.47 to 2.08 ± 0.57) and dV/dt max (2165± 497 to 2207 ± 566) did not change. LV and RV ejection times both fell during NE infusion (LV 139 ± 14 to 116 ± 19 msec, p< 0.02, RV 146 ± 9 to 124 ± 13, p < 0.02), but when adjusted to HR did not change. Thus, even though NE infusion into the LCA selectively enhances LV performance, it does not increase LV SV as compared with the RV. It is concluded that LV and RV ejection in the fetus are largely dependent on loading conditions.