Prevention of postischemic canine neurological injury through potentiation of brain energy metabolism by acetyl-L-carnitine.
- 1 September 1992
- journal article
- abstracts
- Published by Wolters Kluwer Health in Stroke
- Vol. 23 (9) , 1312-1317
- https://doi.org/10.1161/01.str.23.9.1312
Abstract
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.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.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.Postischemic administration of acetyl-L-carnitine potentiates normalization of brain energy metabolites and substantially improves ne...Keywords
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