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In order to determine the cerebral protective effects of an intravenous bolus of 5 mg.kg-1 of lidocaine, the left middle cerebral artery (MCA) was transorbitally occluded in 19 cats. Ten animals received the lidocaine bolus and nine a similar volume of saline immediately before MCA occlusion. Somatosensory evoked potentials (SEP) were recorded before and after the lidocaine bolus as well as continually after MCA occlusion. After six hours of vessel occlusion and without reperfusion, the animals were sacrificed and the brains fixed for histology. Prior to MCA occlusion, lidocaine caused a statistically significant (p less than 0.01) reduction in the amplitude of the major cortical component of the SEP (10 +/- 1.2 microV vs 6.0 +/- 1.3 microV). Latency was unchanged. In the lidocaine group, SEP's persisted in 40 per cent immediately following occlusion whereas they disappeared in all of the control animals (p less than 0.05). Gradual recovery occurred in both groups and there were no differences at the end of the experiment although the amplitudes tended to be greater in the lidocaine group. There were no statistically significant differences in the histological size or severity of the infarcts between the groups. Although infarct size was not reduced, transient sparing of the SEP suggests that further studies of lidocaine by continuous infusion in models of temporary focal cerebral ischaemia may be warranted.

The effects of a prophylactic bolus of lidocaine in focal cerebral ischaemia