title: Plasminogen activation in focal cerebral ischemia and reperfusion.
abstract: In focal cerebral ischemia the plasminogen-plasmin system plays a role in the fibrinolysis of vessel-occluding clots and also in the proteolysis of extracellular matrix components, which potentially contributes to brain edema and bleeding complications. The authors investigated the plasminogen activation after middle cerebral artery occlusion with and without reperfusion (reperfusion intervals 9 and 24 hours) in rats by histologic zymography and compared areas of increased plasminogen activation to areas of structural injury, 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 basal 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 plasminogen 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.
authors.affiliation: Department of Neurology, Klinikum Grosshadern, Ludwig-Maximilians-Universität, Munich, Germany.
authors.forename: T
authors.initials: T
authors.lastname: Pfefferkorn
authors.forename: B
authors.initials: B
authors.lastname: Staufer
authors.forename: M
authors.initials: M
authors.lastname: Liebetrau
authors.forename: G
authors.initials: G
authors.lastname: Bültemeier
authors.forename: M R
authors.initials: MR
authors.lastname: Vosko
authors.forename: C
authors.initials: C
authors.lastname: Zimmermann
authors.forename: G F
authors.initials: GF
authors.lastname: Hamann
mesh_terms: D000818:Animals; D001157:Arterial Occlusive Diseases / Q000378:metabolism; D001479:Basal Ganglia / Q000098:blood supply / Q000737:chemistry / Q000201:enzymology; D001929:Brain Edema / Q000378:metabolism; D002540:Cerebral Cortex / Q000098:blood supply / Q000737:chemistry / Q000201:enzymology; D002543:Cerebral Hemorrhage / Q000378:metabolism; D004195:Disease Models, Animal; D004789:Enzyme Activation; D005341:Fibrinolysin / Q000378:metabolism; D020244:Infarction, Middle Cerebral Artery / Q000378:metabolism*; D002546:Ischemic Attack, Transient / Q000378:metabolism*; D008297:Male; D008869:Microtubule-Associated Proteins / Q000032:analysis / Q000378:metabolism; D010958:Plasminogen / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000378:metabolism*
chemical_list: D008869:Microtubule-Associated Proteins; D010958:Plasminogen; D005341:Fibrinolysin