This study tested the hypothesis that varying degrees of hemodynamic fluctuations seen after birth following immediate cord clamping were related to development of asphyxia with longer cord clamp-to-ventilation intervals, resulting in higher perinatal circulating levels of the catecholamines norepinephrine (NE) and epinephrine (Epi), and thus increased heart rate, blood pressures and cardiac contractility after birth. Anesthetized preterm fetal lambs were instrumented with 1) aortic (AoT) and pulmonary trunk (PT) micromanometers to obtain pressures and the maximal rate of pressure rise (dP/dt_max) as a surrogate measure of ventricular contractility, and 2) an AoT catheter to obtain samples for blood gas and catecholamine analyses. After delivery, immediate cord clamping was followed by ventilation 40sec (n=7), 60sec (n=8), 90sec (n=9) or 120sec later (n=8), with frequent blood sampling performed before and after ventilation. AoT O₂ content fell rapidly after immediate cord clamping (P<0.001), with an asphyxial state evident at ≥60sec. Plasma NE and Epi levels increased progressively with longer cord clamp-to-ventilation intervals, with an exponential relation between falling AoT O₂ content and rising catecholamines (R²=0.64-0.67). Elevated circulating catecholamines persisted for some minutes after ventilation onset, with post-birth surges in heart rate, AoT and PT pressures, and AoT and PT dP/dt_max linearly related to loge of catecholamine levels (R²=0.41-0.54, all P<0.001). These findings suggest that 1) a greater degree of asphyxia-induced sympathoadrenal activation (reflected in elevated circulating catecholamine levels) occurs with longer intervals between immediate cord clamping and subsequent ventilation, and 2) this activation is a major determinant of hemodynamic fluctuations evident with birth.