CAN NIMODIPINE PREVENT ISCHEMIC REPERFUSION INJURY IN THE RAT-BRAIN

Reperfusion injury is a pathophysiological entity distinct from the pr imary ischaemic injury; the oxygen arriving with blood recirculation, although necessary for alleviating the ischaemic status, may be harmfu l and provoke additional injury in the already damaged tissue. This st udy aims to analyse whether nimodipine reduces cerebral dysfunction af ter transient global cerebral ischaemia, using our previously describe d experimental model, which permits the impregnation of cerebral tissu e during the periods of ischaemia and reperfusion. Some aspects of thi s study contribute to our understanding of the reperfusion injury conc ept. Three groups of rats were used. Animals in Group 1 (n = 13) serve d as normal controls for neurophysiological recordings. Rats in Groups 2 (n = 7) and 3 (n = 7) were subjected to global cerebral ischaemia a nd either isotonic saline (Group 2) or nimodipine solution (Group 3; 4 0 mug/kg) was intra-arterially injected through the external carotid a rtery during ischaemia and reperfusion and distributed to the circle o f Willis. Seventy-two hours after global cerebral ischaemia somatosens ory evoked potentials were evaluated and P1 wave latency was used to c ompare the three groups of animals. The peak onset of this wave was 8. 13 +/- 1.5 msec, 18.63 +/- 3.1 msec and 13.17 +/- 2 msec for Groups 1, 2 and 3 respectively. Pl latency was significantly higher in Group 2 than in Groups 1 and 3 (p < 0.01). Histopathological findings showed t hat the level of injury in the hippocampus and striatum in Group 3 was more limited than in Group 2, although no statistical significance co uld be found. There was correlation between neurophysiological finding s and the neuropathological damage observed in the striatum for Groups 2 and 3. It is concluded that the intra-arterial injection of nimodip ine lessens brain damage caused by transient global cerebral ischaemia in rats.