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[Treatment of embolic cerebral infarct via thrombolysis and cytoprotection with U-74389-G in rats].

INTRODUCTION
The best treatment for cerebral ischemic will probably comprise the association of inhibition of ischemia-reperfusion injury mediators and early reperfusion.


OBJECTIVE
We tried to demonstrate if reperfusion by thrombolysis (rt-PA) and free radical scavenging (U-74389-G) reduces ischemic-reperfusion cerebral injury in a rat model of embolic brain infarction.


MATERIAL AND METHODS
39 female Long Evans rats were embolized in right hemisphere with an autologous clot. Three groups are considered; A: control (n = 15), B: rt-PA i.v., 20 mg/kg starting 90-120 minutes after embolization (n = 15), C: rt-PA, same dose, and U-74389-G i.v., 3 mg/kg before and after embolization (n = 9). Arterial blood pressure, gasometry, glycemia and temperature were controlled. Volume of cerebral lesion in surviving animals 24 hours was measured. Autopsy was performed to verify the cause of death in rats which died.


RESULTS
Mortality: group A: 8/15; group B: 9/15; group C: 8/9. Early death was related to cerebral injury except for five rats which developed peritoneal bleeding. We found severe acidosis in rats from group C. Differences in mean volume of ischemic lesion in group A and B are nosignificant despite a tendency to a reduction after thrombolysis.


CONCLUSIONS
In this model thrombolysis alone and in association with U-74389-G failed to reduce cerebral lesion and mortality.