Prevention of cerebral ischaemic reperfusion injury by intra-arterial administration of superoxide dismutase in the rat.

An experimental test was performed to determine whether superoxide dismutase, an oxygen-free radical scavenger, reduces neurological dysfunction after transient global cerebral ischaemia. Three groups of 13 rats each were used. Group 1 served as normal controls. Groups 2 and 3 were subjected to transient global cerebral ischaemia. Before ischaemia, the right carotid bifurcation was isolated and the right external carotid artery was retrogradely cannulated, with the catheter tip positioned near the origin of the internal carotid artery. Once global cerebral ischaemia was complete, either isotonic saline (group 2) or superoxide dismutase solution (group 3) was injected through the above-mentioned catheter, before, during and after reperfusion. Consequently, the injected solutions were distributed through the circle of Willis to all of the ischaemic brain tissue. Somatosensory evoked potentials were registered in the three groups of animals and were used as a measure of neuronal function. In control animals (group 1) mean P1 latency was 8.1 msec and while the mean P1 latency was 11.9 msec in the isotonic saline treated animals (group 2), it was reduced to 8.8 msec in rats treated with the superoxide dismutase solution (group 3). P1 latency was significantly higher in group 2 than in groups 1 and 3 (P less than 0.001). As evaluated by somatosensory evoked potentials, we have concluded that the intra-arterial injection of superoxide dismutase to the ischaemic tissue improves neuronal function in rats subjected to transient global cerebral ischaemia.