Attenuation by acetyl-L-carnitine of neurological damage and biochemical derangement following brain ischemia and reperfusion

Alterations in brain metabolism after ischemia and reperfusion are describe d herein. Several roles played by carnitine and acetylcarnitine can be of p articular relevance in counteracting these brain metabolism alterations. Th e effects of acetyicarnitine in several experimental models of brain ischem ia in rats are described. The data obtained show that acetylcarnitine can h ave significant clinical neuroprotective effects when administered shortly after the onset of focal or global cerebral ischemia. In the canine cardiac arrest model, acetylcarnitine improved the postischemic neurological outco me and tissue levels of lactate and pyruvate were normalized. A trend towar d reversal of pyruvate dehydrogenase inhibition in acetylcarnitine-treated dogs was also observed The immediate postischemic administration of acetylc arnitine prevents free radica-mediated protein oxidation in the frontal cor tex of dogs submitted to cardiac arrest and resuscifation. The transfer of the acetyl group to coenzyme A (CoA) to form acetyl-CoA as the primary sour ce of energy is a plausible mechanism of action of acetyicarnitine.