Tissue plasminogen activator. Reduction of neurologic damage after experimental embolic stroke.
Tissue plasminogen activator (tPA) has become available for pharmacologic use, and it appears to produce relatively fewer hemorrhagic complications than the previously available, less specific thrombolytic agents. We tested the effects of tPA in several models of embolic stroke and found that neurologic damage was reduced when the drug was administered as late as 45 minutes after cerebral embolic occlusion. The mechanism of therapeutic efficacy of tPA was probably thrombolysis. Drug-induced hemorrhages did not occur when therapy was started within four hours after the onset of vascular occlusion. These results suggest that tPA may be useful for thrombolytic therapy of embolic stroke if the drug is administered rapidly after the onset of vascular occlusion.
D000818:Animals; D001921:Brain / Q000473:pathology; D002560:Cerebrovascular Circulation / Q000187:drug effects; D002561:Cerebrovascular Disorders / Q000188:drug therapy* / Q000473:pathology; D004305:Dose-Response Relationship, Drug; D004341:Drug Evaluation; D002542:Intracranial Embolism and Thrombosis / Q000188:drug therapy* / Q000473:pathology; D011817:Rabbits; D013997:Time Factors; D010959:Tissue Plasminogen Activator / Q000008:administration & dosage / Q000627:therapeutic use*
D010959:Tissue Plasminogen Activator