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Stroke, Vol 23, 1312-1317, Copyright © 1992 by American Heart Association

ARTICLES

Prevention of postischemic canine neurological injury through potentiation of brain energy metabolism by acetyl-L-carnitine

RE Rosenthal, R Williams, YE Bogaert, PR Getson and G Fiskum
Department of Emergency Medicine, George Washington University Medical Center, DC 20037.

BACKGROUND AND PURPOSE: Mechanisms of ischemia/reperfusion brain injury include altered patterns of energy metabolism that may be amenable to pharmacological manipulation. The purpose of this study was to test the effectiveness of postischemic acetyl-L-carnitine administration on potentiation of metabolic recovery and prevention of neurological morbidity in a clinically relevant model of complete, global cerebral ischemia and reperfusion. METHODS: Neurological deficit scoring as well as spectrophotometric and fluorescent assays of frontal cortex lactate and pyruvate levels were used in a canine model employing 10 minutes of cardiac arrest followed by restoration of spontaneous circulation for 2 or 24 hours. RESULTS: Dogs treated with acetyl-L-carnitine exhibited significantly lower neurological deficit scores (p = 0.0037) and more normal cerebral cortex lactate/pyruvate ratios than did vehicle-treated control animals. CONCLUSIONS: Postischemic administration of acetyl-L- carnitine potentiates normalization of brain energy metabolites and substantially improves neurological outcome in a clinically relevant model of global cerebral ischemia and reperfusion.

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