HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Correspondence: Submit a response Alert me when this article is cited Alert me when Correspondence are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Dougherty, J. H. Articles by Plum, F. Search for Related Content PubMed PubMed Citation Articles by Dougherty, J. H., Jr. Articles by Plum, F.

Experimental cerebral ischemia produced by extracranial vascular injury

Protection with indomethacin and prostacyclin

Research Center in Cerebrovascular Disease and the Department of Neurology (Drs. Dougherty. Levy. Rawlinson, Ruff, and Plum) and the Division of Hematology. Department of Medicine (Dr. Wekslerl, the New York Hospital-Cornell Medical Center, New York, NY.

To determine whether the production of brain ischemia is modified by antiplatelet agents administered at the time of extracranial endothelial injury, we modified a four-vessel occlusion rat model so that an electrogenic platelet thrombus in one carotid artery produced cerebral ischemia. DC current was passed through an anode around the left carotid artery of 11 rats with preoccluded vertebral and contralateral carotid arteries. Five of six untreated rats became unresponsive because of carotid occlusion and resultant cerebral ischemia; none of five animals pretreated with indomethacin and infused with prostacyclin (PGI₂) were clinically affected. Light-and electronmicroscopic studies showed arterial platelet-fibrin thrombi and ischemic brain damage in untreated rats. All rats had received radiolabeled platelets; radioactivity was increased in the electrogenically injured left carotid arteries from treated and untreated rats, but counts were reduced by more than 80% in indomethacin/ PGL₂-treated rats (p < 0.01).

Address correspondence and reprint requests to Dr. Levy, Department of Neurology, the New York Hospital-Cornell Medical Center, 1300 York Avenue. New York, NY 10021.

This work was supported by NIH Grants Nos. NS-03346 and HL-18828, with additional assistance from NIH Grants Nos. NS-06069 (Dr. Dougherty) and NS-00498 (Dr. Ruff) and an Established Investigator ship from the American Heart Association with funds contributed in part by the New York Heart Association (Dr. Levy).

Presented in part at the thirty-second annual meeting of the American Academy of Neurology. New Orleans. LA, April 1980, and the Tenth Symposium on Cerbral Blood Flow and Metabolism, St. Louis, MO, June 1981.

Accepted for publication February 19, 1982.

This article has been cited by other articles:

				K.-A. Hossmann Experimental models for the investigation of brain ischemia Cardiovasc Res, July 1, 1998; 39(1): 106 - 120. [Full Text] [PDF]

				H. Nagano, T. Suzuki, M. Hayashi, and M. Asano Cerebral Microcirculatory Changes After Cerebral Embolization Induced by Glass Bead Injection in Rabbits Angiology, August 1, 1992; 43(8): 678 - 684. [Abstract] [PDF]