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Introduction: Several studies have indicated that late treatment of aminoguanidine (AG) reduces cerebral ischemic injuries in animal models. However, the effects of early treatment of AG on cerebral ischemic damage are not well understood. This study was designed to evaluate effect of early treatment of AG on cortex and striatum injuries as well as neurological dysfunctions in transient model of focal cerebral ischemia. Methods: Rats (n=30) were assigned to control or AG treated groups (75 or 150 mg/kg, i.p.,). Ischemia was induced by 60 min middle cerebral artery occlusion, followed by 24h reperfusion. Saline (control) or AG were administered at the onset of the ischemia. Twenty-four hours after the end of ischemia, neurological dysfunction scores were determined and then the infarct volumes of cortex and striatum were measured. Results: Administration of AG (75 and 150 mg/kg) at the beginning of ischemia, significantly reduced cortical and striatal infarct volumes by 47%, 69% and 42%, 36%, respectively (p<0.001). Moreover, AG only at dose 150 mg/kg significantly improves neurological dysfunction (p<0.01). Conclusion: Results of this study indicated that administration of AG in early phase of focal cerebral ischemia reduced cortical and striatal infarct volumes and improve neurological deficits in rat model of transient focal cerebral ischemia.

Keywords: Aminoguanidine; Transient focal cerebral ischemia; Rat

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