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Reduction of Neurologic Damage After Experimental Embolic Stroke

Justin A. Zivin, MD, PhD; Patrick D. Lyden, MD; Umberto DeGirolami, MD; Abha Kochhar, PhD; Vincent Mazzarella; C. C. Hemenway, MS; Paul Johnston

Arch Neurol. 1988;45(4):387-391.

Abstract
• 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.

Author Affiliations
From the Neurology Service, Veterans Administration Medical Center and Department of Neurosciences, University of California, San Diego, School of Medicine, La Jolla (Drs Zivin, Lyden, and Kochhar, and Messrs Mazzarella, Hemenway, and Johnston); and the Department of Pathology (Neuropathology), University of Massachusetts Medical Center, Worcester (Dr DeGirolami).

Footnotes
Accepted for publication Jan 11, 1988.

Reprint requests to Department of Neurosciences (M-024), University of California, San Diego, School of Medicine, La Jolla, CA 92093 (Dr Zivin).

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