Prevention of postischemic canine neurological injury through potentiation of brain energy metabolism by acetyl-L-carnitine.
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.[1]References
- Prevention of postischemic canine neurological injury through potentiation of brain energy metabolism by acetyl-L-carnitine. Rosenthal, R.E., Williams, R., Bogaert, Y.E., Getson, P.R., Fiskum, G. Stroke (1992) [Pubmed]
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