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

1992; Lippincott Williams & Wilkins; Volume: 23; Issue: 9 Linguagem: Inglês

10.1161/01.str.23.9.1312

1524-4628

Robert E. Rosenthal, Rebecca E. Williams, Yolanda E. Bogaert, Pamela R. Getson, Gary Fiskum,

Infectious Encephalopathies and Encephalitis

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 neurological outcome in a clinically relevant model of global cerebral ischemia and reperfusion.