Aims: Sympathetic nervous system (SNS) over activity post myocardial infarction (MI) has been implicated in morbidity and mortality. The time course and degree of sympathetic activation and loss of cardiac parasympathetic tone post MI remain unclear in rats. Our aim was to investigate the basal sympathetic activity and its reflex regulation immediately following ligation of the left anterior descending coronary artery (LAD) in the rat. Methods and Results: Experiments were performed in an in situ unanaesthetized decerebrated working heart-brainstem preparation (Paton, 1996) of Wistar rats (60-100g). After baseline recordings of phrenic (PNA) and thoracic sympathetic nerve activities (tSNA), heart rate (HR), ECG and perfusion pressure (PP), either occlusion of the LAD was performed or a sham operation. The myocardial area at risk was assessed post-hoc with Evans Blue dye (0.5%) and was 36.3±1.1% of the left ventricle. One hour after LAD there was: (a) a higher level of tSNA and HR in the LAD rats (from 4.1±0.2 to 6.8±0.5µV, from 343±13 to 352±13bpm, n=21, P<0.01) versus a sham group (from 3.7±0.2 to 3.8±0.3µV, from 321±10 to 326±12.bpm, n=19, P>0.05) (paired t-Test). No changes in PP and respiratory rate (RR) were found between the groups; (b) a greater sympathoexcitatory response to peripheral chemoreceptor stimulation (see Table 1; n=7 each group, P<0.01, unpaired t-Test). No differences in peripheral chemoreflex evoked changes in PP, RR and HR were observed;(c) an elevated pressor response to a bolus injection of phenylephrine (30µg, i.a.) and depressed sympathetic (non-cardiac) baroreflex gain (see Table 2; n=6 each group, P<0.01, unpaired t-Test). The baroreflex bradycardia was unaffected; (d) An elevated cardiac sympathetic tone as assessed with atenolol (20µg/ml) showing a greater fall in HR in LAD rats (-108±8bpm, n=7) compared to sham rats (-82±7bpm; n=5, P<0.05, unpaired t-Test). Cardiac vagal tone was unaffected by LAD. Conclusion: The SNS is activated within minutes after myocardial infarction yet cardiac vagal tone appears unaffected. The mechanisms that produce these initial alterations remain to be investigated.