Gasping is an important autoresuscitative mechanism that is initiated during hypoxia and ischaemia and vital for initiating breathing following a period of apnoea. For this to be effective cardiovascular autonomic motor activity must also be maintained. Recently, we have shown that gasping, but not eupnoea, depends on the integrity of the persistent sodium current, implying that respiratory pacemaker neurones drive gasping (Abdala et al. 2004). Here, we have investigated if sympathetic discharge persists during gasping and whether it is also dependent upon the persistent sodium current. We have employed an in situ arterially perfused preparation of decerebrated rat (the working heart brainstem preparation; Paton, 1996). Decerebration was performed after killing by halothane anaesthesia. We used glass suction electrodes to record from a phrenic nerve, the central end of a vagus nerve and the left thoracic sympathetic chain. To induce gasping, we either induced tissue ischaemia by stopping the perfusion (for 50-70 s) or switched to a perfusate gassed with 5% oxygen and 8% carbon dioxide (for 90-120 s). To block persistent sodium channels, 7 μM riluzole was added to the perfusate since this dose is known to abolish gasping (Abdala et al. 2004). During eupnoea, thoracic sympathetic chain activity typically exhibited discharges that coincided with pre-inspiratory and late inspiratory/early post-inspiratory phases of the respiratory cycle. During gasping (ischaemia, n = 4; hypoxia, n = 4), sympathetic activity exhibited inspiratory related discharges. The sympathetic burst was initiated 0.2-0.6 s prior to the onset of phrenic activity. In addition, baseline tonic sympathetic activity increased by 221.8 ± 43.7% in ischaemia and by 99.0 ± 48.3% in hypoxia compared with eupnoeic levels. Riluzole little affected sympathetic chain and phrenic nerve discharges during eupnoea but abolished gasping. During ischaemia or hypoxia, there was no bursting in the sympathetic chain following riluzole and the evoked increase in tonic basal activity was unaffected compared with control (ischaemia, 189.3 ± 42.5%; hypoxia, 83.6 ± 32.9%). These results suggest that during gasping there is heightened tonic sympathetic discharge and gasp-related bursting occurs. The ischaemia/hypoxia induced increase in tonic sympathetic discharge is not dependent on the persistent sodium current but gasp-related bursting is.