Real-time Detection of Nimodipine Effect on Ischemia Model

摘要

It is generally thought that neuronal damage by cerebral ischemia is associated with extracellular concentrations of the excitatory amino acids. L-glutamate over production initiated the neuronal cell death in ischemic condition. Real time quantitative measurement of glutamate would be applicable to evaluate brain injury during or after surgery, as well as to demonstrate immediate function by Nimodipine, which is one of L-type calcium channel blocker. For in-vivo glutamate measurement, the eleven vessel occlusion (11VO) was prepared by using rat model. Changes in cerebral blood flow were monitored by laser-Doppler flow-metry simultaneously with cortical glutamate level by am-perometric biosensor. Ten minute ischemia was initiated by pulling the snares on the common carotid arteries (CCAs) and the external carotid arteries (ECAs) while Nimodipine was dripped on the vicinity of burr hole for CBF probe during ischemic period. Tn comparison with the Nimodipine-treatment and non-treatment group, peak concentration and the area under the curve (AUC) of glutamate release showed statistically significant difference between two groups. It is considered that decreased glutamate level in Nimodipine treated group is attributed to the neuroprotective effect by Nimodipine.