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There are several other possible mechanisms by which post-ischemic inflammation can disrupt the blood brain barrier (BBB). Inter-endothelial cell tight junctions, the basal lamina, and perivascular astrocytes comprise the blood brain barrier. Following disruption of the endothelium in focal cerebral ischemia, only the basal lamina prevents extravasation of cellular blood elements into the brain parenchyma. Loss of basal lamina integrity results in interstitial edema and 46 Chapter 4 microvascular hemorrhage (23, 24).
Energy failure also leads to depolarization and voltage-dependent loss of magnesium, which normally blocks this receptor (17). Elevated synaptic levels of glutamate lead to large amounts of calcium entering cells (Figure 3-1). Mild hypothermia alters neurotransmitter release (18). During focal cerebral ischemia, neurotransmitter release increases within 10-20 min of ischemia onset, peaks within 60 minutes, decreases by 50-90 min and then returns to baseline or decreases substantially by 90-120 min (18-21).
Busto R, Dietrich WD, Globus MY, et al. Small differences in intraischemic brain temperature critically determine the extent of ischemic neuronal injury. J Cereb Blood Flow Metab 1987; 7:729-738. 24. Kataoka K, Yanase H. Mild hypothermia--a revived countermeasure against isehemic neuronal damages. Neurosci Res 1998; 32: 103-117. 25. Boris-Moller F,Wieloch T. The effect of 4 beta-phorbol-12,13-dibutyrate and staurosporine on the extracellular glutamate levels during ischemia in the rat striatum.