Abstract
Cerebral ischemia in Monogolian gerbil (Meriones unguiculatus) results in an acute “energy crisis” followed by the marked changes in monoamines; norepinephrine is the first to be depleted in cerebral ischemia (6). In spite of a lot of data about the fate of monoamines in ischemia, only a few studies have evaluated the metabolism of amines in reflow (1, 7). Moreover, evidence is lacking about the regional changes of catecholamines and related degradative enzymes during longterm reflow after the transient ischemic attack. The data presented here reveal the alterations of the catecholamine and their degradative enzymes during long-term reflow; a pattern of oscillatory behavior of both amines and enzymes was evident in postischemia. Thus, the disorder of catecholamine metabolism in the ischemic brain and during the postischemic period perhaps contributes to the neurological dysfunction which follows an ischemic insult.
Published Version
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