Plasminogen activation in focal cerebral ischemia and reperfusion

In focal cerebral ischemia the plasminogenplasmin system plays a role in th e fibrinolysis of vessel-occluding clots and also in the proteolysis of ext racellular matrix components, which potentially contributes to brain edema and bleeding complications. The authors investigated the plasminogen activa tion after middle cerebral artery occlusion with and without reperfusion (r eperfusion intervals 9 and 24 hours) in rats by histologic zymography and c ompared areas of increased plasminogen activation to areas of structural in jury, which were detected immunohistochemically. After 3 hours of ischemia, increased plasminogen activation was observed in the ischemic hemisphere, The affected area measured 5.2% +/- 8.5% and 19.4% +/- 30.1% of the total b asal ganglia and cortex area, respectively. Reperfusion for 9 hours after 3 hours of ischemia led to a significant expansion of plasminogen activation in the basal ganglia (68.8% +/- 42.2%, P < 0.05) but not in the cortex (43 .0% +/- .34.6%, P = 0.394), In the basal ganglia, areas of increased plasmi nogen activation were related to areas of structural injury (r = 0.873, P < 0.001). No such correlation was found in the cortex (r = 0.299, P = 0.228) , In this study, increased plasminogen activation was demonstrated early in focal cerebral ischemia. This activation may promote early secondary edema formation and also secondary hemorrhage after ischemic stroke.