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John M. Hallenbeck, MD; Andrew J. Dutka, MD

Arch Neurol. 1990;47(11):1245-1254.

Abstract
• We define the concept of reperfusion injury, and we present a background chronology of experimental work supporting and questioning this concept. We identify several new influences, such as current clinical interest in thrombolytic therapy for acute ischemia of heart and brain and the growing recognition of endothelium as a regulator of homeostasis. We propose that these influences will encourage a reexamination of reperfusion injury as a factor in the ultimate outcome of tissue exposed to reversible ischemia. We briefly discuss the major mechanisms presently implicated in reperfusion injury—loss of calcium homeostasis, free radical generation, leukocyte-mediated injury, and acute hypercholesterolemia.

Author Affiliations
From the Neurology Department, National Naval Medical Center, Bethesda, Md.

Footnotes
Accepted for publication April 30, 1990.

The opinions and assertions contained herein are the private ones of the authors and are not to be construed as official or reflecting the views of the Navy Department or the Naval Service at large.

Reprint requests to Neurology Department, National Naval Medical Center, 8901 Wisconsin Ave, Bethesda, MD 20814-5011 (Dr Hallenbeck).

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