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Rat Model of Blood-brain Barrier Disruption to Allow Targeted Neurovascular Therapeutics
Published on: November 30, 2012
The selective Na+-Ca2+ exchange inhibitor attenuates brain edema after radiofrequency lesion in rats
Yutaka Koyama1, Shigeo Matsui, Soichi Itoh
1Laboratory of Medicinal Pharmacology, Graduate School of Pharmaceutical Sciences, Osaka University, 1-6 Yamada-oka, Suita, Osaka 565-0871, Japan.
Abstract:
2-[4-[(2,5-Difluorophenyl)methoxy]phenoxy]-5-ethoxyaniline (SEA0400), a specific inhibitor of the Na+-Ca2+ exchanger, exerts cytoprotective action and reduces brain infarct volume after cerebral ischemia. We examined the effect of SEA0400 on vasogenic brain edema in rats. Histological observations showed that radiofrequency current caused brain infarct and extravasation of endogenous albumin in the brain. SEA0400 (3 and 10 mg/kg, i.v.) significantly suppressed the increase in brain water content with attenuation of Evans blue dye and sodium fluorescein extravasation after radiofrequency lesion. The findings suggest that the Na+-Ca2+ exchanger plays a role in vasogenic edema formation after radiofrequency lesion.

