LAUSR

BACKGROUND Dispersion in ventricular repolarization is relevant for arrhythmogenesis. OBJECTIVE To determine the spatiotemporal effects of sympathetic stimulation on ventricular repolarization. METHODS In five anesthetized female open chested pigs ventricular repolarization was measured from the anterior, lateral and posterior wall of the left (LV) and right ventricle (RV) using up to 40 transmural plunge needles (4 electrodes each), before and after left and right stellate stimulation (LSGS and RSGS). In addition, LSGS was performed in 3 pigs (2 male, 1 female) before and after verapamil (5-10 mg/hr) administration. RESULTS LSGS yielded a biphasic response in repolarization in the lateral and posterior wall of the LV, with prolongation at ∼5 seconds (+10±1.5 ms) and a shortening at 20-30 seconds of stimulation (-28.9±4.4 ms) during a monotonic pressure increase. While the initial prolongation was abolished by verapamil, the late shortening was augmented. Sequential transections of the vagal nerve and stellate ganglia augmented repolarization dispersion responses to LSGS in 2 out of 5 hearts. An equal pressure increase by aortic occlusion resulted in a homogeneous shortening of repolarization in the LV and the effects were smaller than during LSGS. RSGS shortened repolarization mainly in the anterior LV wall, but the effects were smaller than those of LSGS. CONCLUSION LSGS first prolongs (through the L-type calcium current) and then shortens repolarization. The effect of LSGS was prominent in the posterior and lateral, not the anterior, LV wall.