SE also induces severe vasogenic edema in the PC accompanied by neuronal and astroglial damages [5-8]. Brain edema proceeds in two phases, early cytotoxic edema phase and late vasogenic edema phase. Early cytotoxic osmotic edema is due to excess stimulation of glutamatergic pathways during SE, which increases intracellular Na+ and Ca2+ concentrations. The vasogenic edema results from dysfunction of endothelial cells and the blood-brain barrier (BBB). Many studies have reported increased permeability of the BBB during epileptic activity [9-13]. A fast and significant increase in systemic blood pressure, particularly shown during tonic epileptic seizures, induces a marked vasodilation of the large cerebral arteries and an increase in blood pressure in capillaries, small arteries, and veins leading to leakage of the BBB [9]. Loss of BBB integrity is not only due to an abrupt increase in the intraluminal pressure but also influenced by the properties of cerebral tissue. Indeed, an acute increase in blood pressure or epileptic activity causes an increase in pinocytosis at the level of the cerebral endothelium [11-13].