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      Tissue plasminogen activator mediated blood-brain barrier damage in transient focal cerebral ischemia in rats: relevance of interactions between thrombotic material and thrombolytic agent.

      Vascular Pharmacology
      Animals, Basal Ganglia, pathology, Blood-Brain Barrier, drug effects, physiology, Brain, Evans Blue, Fibrinolytic Agents, pharmacology, Immunohistochemistry, Ischemic Attack, Transient, Laser-Doppler Flowmetry, Male, Matrix Metalloproteinase 9, biosynthesis, metabolism, Rats, Rats, Wistar, Reperfusion Injury, physiopathology, Thrombosis, Tissue Plasminogen Activator

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          Abstract

          Thrombolysis with tPA for acute ischemic stroke is associated with an increased risk of intracerebral hemorrhage. We investigated the impact of thrombolysis with tPA on the blood-brain barrier in a suture occlusion model in rats. Cerebral ischemia was performed for 2 h followed by 22 h of reperfusion. Treatment groups received either saline (A), 10 mg/kg bw rtPA (B) or "activated" rtPA (ArtPA, C, rtPA with in vitro clot contact). Blood-brain-barrier damage assessed by Evans blue extravasation as a permeability marker was significantly enhanced in basal ganglia of group C compared to groups A or B. Likewise was the upregulation of MMP-9. Interestingly, results of the rtPA and saline group showed only minor and not statistically significant differences. The results of the present study indicate a major role for thrombus-thrombolytic interaction in focal cerebral ischemia with subsequent increased BBB permeability.

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