• Abedin Vakili, Fezzeh Hosseinzadeh, and Toktam Sadogh.
• University of Medical Sciences, Seman, Iran. Abvakili@yahoo.com
• Brain Res. 2007 Sep 19; 1170: 97-102.

AbstractPrevious experimental studies have shown that aminoguanidine (AG) is beneficial in the late phase of cerebral ischemia. Recently, it has been reported that AG reduces cerebral edema in traumatic brain injury. However, the effects of AG on post-ischemic cerebral edema and blood-brain barrier (BBB) permeability are not clear. Under chloral hydrate anesthesia, transient focal cerebral ischemia was induced in rats by 60 min of middle cerebral artery occlusion (MCAO), followed by 23 h of reperfusion. Saline as vehicle or AG at the doses of 75, 150 and 300 mg/kg, i.p., was administered at the beginning or at 1 or 3 h after induction of ischemia. Subsequently, 24 h after MCAO brain edema, BBB permeability and infarct volume were evaluated. Administration of AG (150 mg/kg) at the beginning or at 1 or 3 h after MCAO, significantly reduced cerebral edema (P<0.001), while AG at the doses of 75 and 300 mg/kg had no effect. Moreover, treatment with AG (150 mg/kg) significantly reduces Evans Blue extravasation by 48% into ischemic brain compared to the saline group (P<0.001). Additionally, AG at the doses of 75 and 150 mg/kg significantly reduces cortical and striatal infarct volumes (P<0.001), while AG at the dose of 300 mg/kg did not change striatal infarct volumes (P>0.05). Our findings show that AG significantly reduced post-ischemic increase of brain edema with a 3-h therapeutic window in the transient model of focal cerebral ischemia. Moreover, it seems that at least part of the anti-edematous effects of AG is due to decrease of BBB disruption.

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