Abnormal cardiac autonomic innervation may be a mechanism leading to sudden infant death syndrome (SIDS). The present study evaluated the influence of selected cardiac denervations on ventricular fibrillation threshold (VFT) in one month old swine. Saffan-anesthetized, open-chest swine were artificially ventilated with 100% O2. Aortic pressure (AoP) and ECG (Lead II) were recorded. For VFT measurement, a train of 10 pulses of 10 msec duration at 20 Hz was delivered through bipolar electrodes positioned at the apex of the heart. Current intensity was progressively increased by 0.5 mA until ventricular fibrillation occurred. The lowest current intensity, which induced fibrillation, was defined as VFT. Defibrillation was accomplished within 15 sec following fibrillation. The VFT measurement was repeated 30 min later following recovery of the ECG, AoP, blood gases and pH. In sham control: 1st VFT= 4.8 ± 1.0 mA vs 2nd VFT = 4.4 ± 1.6 mA, Mean ± SD, n=5, p>0.05. For the denervation groups (with vagi intact): VFT was measured pre- and 30 min post right stellate ganglionectomy (RSG) or left stellate ganglionectomy (LSG) or bilateral stellate ganglionectomy (BSG). There were significant decreases in VFT following RSG (5.0 ± 1.3 vs 2.9± 1.3 mA, p<0.05, n=6) but not following LSG (5.0 ± 0.8 vs 4.6 ± 1.6 mA, n=7, p>0.05) or BSG (5.30 ± 1.8 vs 5.24± 1.9 mA, n=8, p>0.05). The results suggest that elimination of the right stellate (left-sided dominance) increase susceptibility to ventricular fibrillation while elimination of the left or both stellates in the swine did not alter VFT. Thus we speculate that inappropriate development of cardiac autonomic innervation in the neonate may be a mechanism in the etiology of SIDS.(Supported by NIH grant HD-28931).