抄録
In this study, the thrombotic occlusion of the middle cerebral artery (MCA) was induced by photochemical reaction between Rose Bengal and green light which causes endothelial injury followed by platelet adhesion, aggregation and formation of a platelet and fibrin-rich thrombus at the site of photochemical reaction. Using this model, we have investigated effects of antithrombotic agents, thrombolytic agents and neuroprotective agents. A thromboxane A2 receptor antagonist, ADP-induced platelet aggregation inhibitor and a selective thrombin inhibitor-inhibited the MCA thrombogenesis, suggesting that platelets play a key role in MCA thrombosis in this model. A tissue-type plasminogen activator (tPA), administered intravenously 30 min after the MCA occlusion could induce reopening of the thrombotically occluded artery, resulting in reduction of cerebral infarction size 24 h after the tPA administration. A glutamate release inhibitor and AMPA/kainate receptor antagonist, administered after the MCA occlusion reduced the size of cerebral infarction 24 h after the MCA occlusion. Using a microdialysis technique, glutamate concentration in the ischaemic border zone was measured and glutamate release was induced following cerebral ischaemia. This suggests that an increase in glutamate concentration in ischaemic border zone may play a key role in the development of cerebral infarction.
